By Kyle J. Norton
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
Type II diabetesDiabetes is defined as a medical condition of insufficient insulin entering the bloodstream to regulate the glucose. It is either caused by cells in the pancreas dying off or receptor sites clogged up by the accumulation of fat and cholesterol. In some case, diabetes is also caused by allergy reactions of cells in our body.
How do calculate your BMI indexBMI= weight (kg)/ height (m2)
How obesity cause type II diabetes
Type II diabetes is a result of insulin resistance and obesity is considered as a risk factor for developing insulin resistance.
1. According to the article of "Obesity and insulin resistance" by Barbara B. Kahn and Jeffrey S. Flier (1), researchers indicated that the association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental aspect of the etiology of type 2 diabetes and is also linked to a wide array of other pathophysiologic sequelae including hypertension, hyperlipidemia, atherosclerosis (i.e., the metabolic syndrome, or syndrome X), and polycystic ovarian disease.
1. Can Gene and Inherited factor cause of Obesity and type II diabetes be changed
Obesity and type II diabetes as a result of genetic susceptible or heredity can be prevented, according to the study of " Lifestyle and Genetics in Obesity and type 2 Diabetes." by Temelkova-Kurktschiev T, Stefanov T. (Source from Medicobiological Unit.) posted in PubMed, researchers found that gene-lifestyle interaction studies suggest that
a. Genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease.
b. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future.
By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.
2. Leptin and Obesity and Type 2 Diabetes
Since leptin is the protein product of the obese gene, many researchers have tries to develop the mew approach to treat obesity and type 2 diabetes. In a study of " Novel Approaches to the Treatment of Obesity and Type 2 Diabetes Mellitus: Bioactive Leptin-Related Synthetic Peptide Analogs." by Grasso P. (Source from Department of Medicine, Division of Endocrinology and Metabolism Albany Medical College, MC 141, Albany, NY 12208, USA. grassop@mail.amc.edu), posted in PubMed, researches indicated that The pleiotropic nature of leptin has been confirmed by demonstration of a role for leptin in hematopoiesis, angiogenesis, immune function, osteogenesis, reproduction, and wound healing. Unfortunately, the results of the majority of clinical trials with recombinant human leptin indicated that its effectiveness in restoring energy balance and correcting obesity-related endocrinopathies in genetically obese rodent models extended only to the management of those rare forms of human obesity caused by mutation in the ob gene. Failure of leptin in the clinic, and withdrawal of fenfluramine, phentermine, and sibutrimine from clinical use in the United States, have stimulated new approaches in the development of anti-obesity and anti-diabetes pharmacophores.
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(1) Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USAAddress correspondence to: Barbara B. Kahn, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: (617) 667-5422; Fax: (617) 667-2927; E-mail: bkahn@caregroup.harvard.edu. The Journal of Clinical investigation
Saturday 9 August 2014
The recipe 4 nut and seed lovers: Spiced chili nuts and seeds
Recipe contributed by Fresh and Easy Meals by Better Homes and Gardens
Pick your favorite nuts and seed for this snack recipe. Orange juice concentration spiked with piquant spices gives the mixture a burst of favor.
Prep. 10 minutes
Bake 15 minutes
Oven 300 degrees F
Make 16 (1/4 cup) serving
2 tsp. frozen orange juice concentrate thawed.
2 tsp. Worcestershire sauce
1 tsp. garlic powder
1 tsp. ground cumin
1 tsp. chili powder
1/2 tsp. cayenne pepper
1/4 tsp. salt
1/4 tsp. ground allspice
1.4 tsp. onion salt
2 cups unsalted peanuts, hazelnuts, and/or Brazil nuts
1 cup pecan halves
6 tsp. unsalted shelled sunflower seeds
2 tsp. sesame seeds
Non stick cooking tray
In a large bowl, combined orange juice concentrate, Worcestershire sauce, garlic powder, cumin, chili powder, cayenne pepper,salt, allspice, black pepper and onion salt. Stir in nuts and seeds; toss to coat.
Line a 15x10x1 inch baking pan with foil; slightly coat with nonstick cooking spray. Spread nuts and seed on foil. Bake in a300 degrees oven for 15 to 20 minutes or until toasted, stirring once. Cool. Store in an airtight container at room temperature for up to 1 week.
Nutrition facts per serving: 186Cal, 16 g total fat(2 g sat. fat), 0mg cholesterol, 59 sodium, 7 g carbo, 3 g fiber, 6 g pro.
daily value: 2% vitamin A, 6% vitamin C, 2% calcium, 5% iron.
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Pick your favorite nuts and seed for this snack recipe. Orange juice concentration spiked with piquant spices gives the mixture a burst of favor.
Prep. 10 minutes
Bake 15 minutes
Oven 300 degrees F
Make 16 (1/4 cup) serving
2 tsp. frozen orange juice concentrate thawed.
2 tsp. Worcestershire sauce
1 tsp. garlic powder
1 tsp. ground cumin
1 tsp. chili powder
1/2 tsp. cayenne pepper
1/4 tsp. salt
1/4 tsp. ground allspice
1.4 tsp. onion salt
2 cups unsalted peanuts, hazelnuts, and/or Brazil nuts
1 cup pecan halves
6 tsp. unsalted shelled sunflower seeds
2 tsp. sesame seeds
Non stick cooking tray
In a large bowl, combined orange juice concentrate, Worcestershire sauce, garlic powder, cumin, chili powder, cayenne pepper,salt, allspice, black pepper and onion salt. Stir in nuts and seeds; toss to coat.
Line a 15x10x1 inch baking pan with foil; slightly coat with nonstick cooking spray. Spread nuts and seed on foil. Bake in a300 degrees oven for 15 to 20 minutes or until toasted, stirring once. Cool. Store in an airtight container at room temperature for up to 1 week.
Nutrition facts per serving: 186Cal, 16 g total fat(2 g sat. fat), 0mg cholesterol, 59 sodium, 7 g carbo, 3 g fiber, 6 g pro.
daily value: 2% vitamin A, 6% vitamin C, 2% calcium, 5% iron.
Weight Loss the Easy Ways
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4 the best soup with Vegetable stock
Recipe contributed by 125 Chinese recipes with Bill Jones and Stephen Wong
4 large onions, peeled and roughly chopped
2 leeks, washed and roughly chopped
5 stalks of celery, roughly chopped
3 bay leaves
1 small mixed herb (cilantro, basil, etc.)
10 whole pepper corns
1/2 head garlic
2 ginger slices
1 tsp. fennel seed
1 tsp. whole allspice
1 tsp. whole coriander seed
2 cups white wine
20 cups water
1. Place ingredients in a large stockpot, adding more water, if necessary to cover. Bring mixture to a broil; reduce heat and simmer gently for 2 hours, skimming occasionally to remove any foam or impurities that rise to the top. Try not to let the mixture boil or broth will be cloudy.
2. strain in to container and cool to room temperature before refrigerating. (If hot stock is placed directly in the fridge, it will sometime sour). for a more intensely flavored stock, let liquid cool; return stock to pot and over low heat, simmer until volume is reduced by half.
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4 large onions, peeled and roughly chopped
2 leeks, washed and roughly chopped
5 stalks of celery, roughly chopped
3 bay leaves
1 small mixed herb (cilantro, basil, etc.)
10 whole pepper corns
1/2 head garlic
2 ginger slices
1 tsp. fennel seed
1 tsp. whole allspice
1 tsp. whole coriander seed
2 cups white wine
20 cups water
1. Place ingredients in a large stockpot, adding more water, if necessary to cover. Bring mixture to a broil; reduce heat and simmer gently for 2 hours, skimming occasionally to remove any foam or impurities that rise to the top. Try not to let the mixture boil or broth will be cloudy.
2. strain in to container and cool to room temperature before refrigerating. (If hot stock is placed directly in the fridge, it will sometime sour). for a more intensely flavored stock, let liquid cool; return stock to pot and over low heat, simmer until volume is reduced by half.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
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Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple WaySuper foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
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Friday 8 August 2014
Obesity Complication of Insulin Resistance
By Kyle j. Norton
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Insulin Resistance is defined as condition of the pancreas has become less effective in lowering the glucose in the blood that can lead to diabetes and other health problems, such as coronary artery disease, stroke, and type 2 diabetes.
How Obesity associates with Insulin Resistance
1. According to the study of "Inflammatory mediators and insulin resistance in obesity: role of nuclear receptor signaling in macrophages?" by Fuentes L, Roszer T, Ricote M., posted in PubMed, researchers found that Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.
2. In the study of "Association studies of novel obesity-related gene variants with quantitative metabolic phenotypes in a population-based sample of 6,039 Danish individuals" by Burgdorf KS, Gjesing AP, Grarup N, Justesen JM, Sandholt CH, Witte DR, Jørgensen T, Madsbad S, Hansen T, Pedersen O., posted in PubMed, researchers found that Our correlative findings from analysing single-locus data suggest that some variation in validated BMI and WHR loci are associated with either increased or decreased insulin sensitivity and thereby potentially with metabolically healthy or metabolically unhealthy subsets of obesity. The results call for testing in larger study samples and for further physiological exploration of the possible metabolic implications of these loci.
3. According to the abstract of the study of 'Polymorphisms in the adiponutrin gene are associated with increased insulin secretion and obesity" by Johansson LE, Lindblad U, Larsson CA, Råstam L, Ridderstråle M., posted in PubMed, researchers concluded that We confirm the association between PNPLA3 and obesity. In addition, the rs738409 variant was associated with insulin secretion. There seems to be a differential effect of the Ile-allele depending on the degree of obesity, possibly as a consequence of insulin resistance.
4. In the study of "Association analysis indicates that a variant GATA-binding site in the PIK3CB promoter is a Cis-acting expression quantitative trait locus for this gene and attenuates insulin resistance in obese children" by Le Stunff C, Dechartres A, Mariot V, Lotton C, Trainor C, Miraglia Del Giudice E, Meyre D, Bieche I, Laurendeau I, Froguel P, Zelenika D, Fallin D, Lathrop M, Roméo PH, Bougnères P., posted in PubMed, researchers filed the conclusion that the C allele of rs361072 is a causal variant capable of attenuating insulin resistance in obese children through increased expression of p110beta.
5. According to the study of "Genetics of insulin resistance" by Pedersen O., posted in PubMed, researcher indicated that Even among young, healthy individuals, there is more than a 10-fold variation in insulin sensitivity; however, taken in combination, all the known modifiers of insulin sensitivity - including obesity and a variety of environmental factors - explain less than one third of this variation........ and concluded that It is likely that inherited insulin resistance will eventually prove to be related to subtle mutations in many such genes of the insulin signalling network and the numerous genetic components controlling energy metabolism.
6. In another study of "Insulin resistance: interactions between obesity and a common variant of insulin receptor substrate-1" by Clausen JO, Hansen T, Bjørbaek C, Echwald SM, Urhammer SA, Rasmussen S, Andersen CB, Hansen L, Almind K, Winther K, et al., posted in PubMed, researchers found that The obese carriers of the codon-972 variant were also characterised by a clustering of metabolic cardiovascular risk factors, with raised fasting concentrations of plasma glucose, serum triglyceride, and plasma tissue-plasminogen-activator and its fast-acting inhibitor. With adjustment for known modulators of insulin sensitivity, multivariate analyses showed that the combination of obesity and the codon-972 variant was associated with a 50% reduction in insulin sensitivity (p = 0.0008). Our results suggest that the codon-972 IRS-1 gene variant may interact with obesity in the pathogenesis of common insulin-resistant disorders.
7. Etc.
Treatments of Obesity and Insulin Resistance
1. In the abstract of the study of "Molecular mechanism of insulin resistance in obesity and type 2 diabetes" by Choi K, Kim YB., posted in PubMed, researchers indicated that Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resistance in obesity and type 2 diabetes. In addition, the effects of insulin-sensitizing agent treatment and lifestyle intervention of human insulin-resistant subjects on insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a newly identified regulator of insulin action in insulin control of metabolism, is addressed.
2. In a study of "Insulin resistance and improvements in signal transduction" by Musi N, Goodyear LJ., posted in PubMed, researchers stated that A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. AMP-activated protein kinase (AMPK) is an enzyme that works as a fuel gauge and becomes activated in situations of energy consumption, such as muscle contraction. Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Moreover, in the hypothalamus, AMPK regulates appetite and body weight. The effect of AMPK to stimulate muscle glucose disposal and to control appetite makes it an important pharmacologic target for the treatment of type 2 diabetes and obesity.
3. According to another study of "Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance" by Hawley JA., posted in PubMed, researcher indicated that During the past half-century, there has been a dramatic increase in the incidence of obesity, insulin resistance and type 2 diabetes....... Several putative mechanisms for enhanced glucose uptake after exercise training will be discussed. A determination of the underlying biological mechanisms that result from exercise training is essential in order to define the precise variations in physical activity that result in the most desired effects on targeted risk factors, and to aid in the development of such interventions.
4. In a study of "Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance" by Trovato GM, Martines GF, Trovato FM, Pirri C, Pace P, Garozzo A, Castro A, Catalano D., posted in PubMed, researchers concluded that Ad36 previous infection is significantly associated with enhanced weight loss, bright liver disappearance, and recovery of insulin sensitivity through the chosen tailored nutritional interventional treatment. Nonetheless, Ad36 seronegative NAFLD patients' fatty liver pattern improves, at a lower extent, also without significant weight loss: an effect of dietary changes profile, Mediterranean diet, not only of lowered food caloric intake, is conceivably operating.
5. Etc.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Insulin Resistance is defined as condition of the pancreas has become less effective in lowering the glucose in the blood that can lead to diabetes and other health problems, such as coronary artery disease, stroke, and type 2 diabetes.
How Obesity associates with Insulin Resistance
1. According to the study of "Inflammatory mediators and insulin resistance in obesity: role of nuclear receptor signaling in macrophages?" by Fuentes L, Roszer T, Ricote M., posted in PubMed, researchers found that Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.
2. In the study of "Association studies of novel obesity-related gene variants with quantitative metabolic phenotypes in a population-based sample of 6,039 Danish individuals" by Burgdorf KS, Gjesing AP, Grarup N, Justesen JM, Sandholt CH, Witte DR, Jørgensen T, Madsbad S, Hansen T, Pedersen O., posted in PubMed, researchers found that Our correlative findings from analysing single-locus data suggest that some variation in validated BMI and WHR loci are associated with either increased or decreased insulin sensitivity and thereby potentially with metabolically healthy or metabolically unhealthy subsets of obesity. The results call for testing in larger study samples and for further physiological exploration of the possible metabolic implications of these loci.
3. According to the abstract of the study of 'Polymorphisms in the adiponutrin gene are associated with increased insulin secretion and obesity" by Johansson LE, Lindblad U, Larsson CA, Råstam L, Ridderstråle M., posted in PubMed, researchers concluded that We confirm the association between PNPLA3 and obesity. In addition, the rs738409 variant was associated with insulin secretion. There seems to be a differential effect of the Ile-allele depending on the degree of obesity, possibly as a consequence of insulin resistance.
4. In the study of "Association analysis indicates that a variant GATA-binding site in the PIK3CB promoter is a Cis-acting expression quantitative trait locus for this gene and attenuates insulin resistance in obese children" by Le Stunff C, Dechartres A, Mariot V, Lotton C, Trainor C, Miraglia Del Giudice E, Meyre D, Bieche I, Laurendeau I, Froguel P, Zelenika D, Fallin D, Lathrop M, Roméo PH, Bougnères P., posted in PubMed, researchers filed the conclusion that the C allele of rs361072 is a causal variant capable of attenuating insulin resistance in obese children through increased expression of p110beta.
5. According to the study of "Genetics of insulin resistance" by Pedersen O., posted in PubMed, researcher indicated that Even among young, healthy individuals, there is more than a 10-fold variation in insulin sensitivity; however, taken in combination, all the known modifiers of insulin sensitivity - including obesity and a variety of environmental factors - explain less than one third of this variation........ and concluded that It is likely that inherited insulin resistance will eventually prove to be related to subtle mutations in many such genes of the insulin signalling network and the numerous genetic components controlling energy metabolism.
6. In another study of "Insulin resistance: interactions between obesity and a common variant of insulin receptor substrate-1" by Clausen JO, Hansen T, Bjørbaek C, Echwald SM, Urhammer SA, Rasmussen S, Andersen CB, Hansen L, Almind K, Winther K, et al., posted in PubMed, researchers found that The obese carriers of the codon-972 variant were also characterised by a clustering of metabolic cardiovascular risk factors, with raised fasting concentrations of plasma glucose, serum triglyceride, and plasma tissue-plasminogen-activator and its fast-acting inhibitor. With adjustment for known modulators of insulin sensitivity, multivariate analyses showed that the combination of obesity and the codon-972 variant was associated with a 50% reduction in insulin sensitivity (p = 0.0008). Our results suggest that the codon-972 IRS-1 gene variant may interact with obesity in the pathogenesis of common insulin-resistant disorders.
7. Etc.
Treatments of Obesity and Insulin Resistance
1. In the abstract of the study of "Molecular mechanism of insulin resistance in obesity and type 2 diabetes" by Choi K, Kim YB., posted in PubMed, researchers indicated that Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resistance in obesity and type 2 diabetes. In addition, the effects of insulin-sensitizing agent treatment and lifestyle intervention of human insulin-resistant subjects on insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a newly identified regulator of insulin action in insulin control of metabolism, is addressed.
2. In a study of "Insulin resistance and improvements in signal transduction" by Musi N, Goodyear LJ., posted in PubMed, researchers stated that A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. AMP-activated protein kinase (AMPK) is an enzyme that works as a fuel gauge and becomes activated in situations of energy consumption, such as muscle contraction. Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Moreover, in the hypothalamus, AMPK regulates appetite and body weight. The effect of AMPK to stimulate muscle glucose disposal and to control appetite makes it an important pharmacologic target for the treatment of type 2 diabetes and obesity.
3. According to another study of "Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance" by Hawley JA., posted in PubMed, researcher indicated that During the past half-century, there has been a dramatic increase in the incidence of obesity, insulin resistance and type 2 diabetes....... Several putative mechanisms for enhanced glucose uptake after exercise training will be discussed. A determination of the underlying biological mechanisms that result from exercise training is essential in order to define the precise variations in physical activity that result in the most desired effects on targeted risk factors, and to aid in the development of such interventions.
4. In a study of "Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance" by Trovato GM, Martines GF, Trovato FM, Pirri C, Pace P, Garozzo A, Castro A, Catalano D., posted in PubMed, researchers concluded that Ad36 previous infection is significantly associated with enhanced weight loss, bright liver disappearance, and recovery of insulin sensitivity through the chosen tailored nutritional interventional treatment. Nonetheless, Ad36 seronegative NAFLD patients' fatty liver pattern improves, at a lower extent, also without significant weight loss: an effect of dietary changes profile, Mediterranean diet, not only of lowered food caloric intake, is conceivably operating.
5. Etc.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
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Crispy Parmesan Pita Crackers
Contributed by Quick and easy family favorites by Vickie and JoAnn
These is great salad and dips. For added flavor, sprinkle with garlic powder herbs before baking.
5 pita round
non-stick vegetable spray
1/2 c. grated Parmesan cheese
Split pitas and cut each half into wedges. Arrange on a baking sheet; spray lightly with non- stick vegetable spray and sprinkle with grated Parmesan. bake at 450 degrees for 8 to 10 minutes or until crisp.
make 5 dozen.
Laura Fuller
Fort Wayne, IN
Weight Loss the Easy Ways
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will Personally Coach You How to Get There The Easy Way
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At Last! The Natural PCOS Diet
A Naturopath’s Easy Step-by-Step Guide to Overcome PCOS
by Qualified Australian Naturopath And Hormone Health Expert
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These is great salad and dips. For added flavor, sprinkle with garlic powder herbs before baking.
5 pita round
non-stick vegetable spray
1/2 c. grated Parmesan cheese
Split pitas and cut each half into wedges. Arrange on a baking sheet; spray lightly with non- stick vegetable spray and sprinkle with grated Parmesan. bake at 450 degrees for 8 to 10 minutes or until crisp.
make 5 dozen.
Laura Fuller
Fort Wayne, IN
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
At Last! The Natural PCOS Diet
A Naturopath’s Easy Step-by-Step Guide to Overcome PCOS
by Qualified Australian Naturopath And Hormone Health Expert
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
The Tongue appreciated recipe: Home style 5 spice mix
Recipe contributed by 125 Chinese recipes with Bill Jones and Stephen Wong
2 tbsp. fennel seeds
2 tbsp. clove sticks
2 tbsp. star rinse
2 tbsp. Szechuan peppercorns
2 cinnamon sticks
1. In a nonstick pan over medium heat, cook the spices, shaking the pan constantly. When the pan just begins to smoke, remove from heat transfer contents to a place to cool.
2 In a small coffee or spice grinder (you can also use a mortar and pestle or blender or food processor) grind spices until a fine powder is obtained. transfer to a small, sealable plastic container and reserve until needed
Weight Loss the Easy Ways
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2 tbsp. fennel seeds
2 tbsp. clove sticks
2 tbsp. star rinse
2 tbsp. Szechuan peppercorns
2 cinnamon sticks
1. In a nonstick pan over medium heat, cook the spices, shaking the pan constantly. When the pan just begins to smoke, remove from heat transfer contents to a place to cool.
2 In a small coffee or spice grinder (you can also use a mortar and pestle or blender or food processor) grind spices until a fine powder is obtained. transfer to a small, sealable plastic container and reserve until needed
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Super foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
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Thursday 7 August 2014
Obesity Complication of Non-alcoholic Fatty Liver Disease
By Kyle J. Norton
Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Non-alcoholic Fatty Liver Disease is defined as a condition of the fatty liver diseases as a result of accumulated of fat in the liver, not caused by abusive alcohol consumption. According to the study of "Nonalcoholic Fatty Liver Disease An Underrecognized Cause of Cryptogenic Cirrhosis" by Jeanne M. Clark, MD, MPH, Anna Mae Diehl, MD, posted in The Journals of the American Medical Association, researchers indicated in abstract that Cryptogenic cirrhosis is a common cause of liver-related morbidity and mortality in the United States. Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most common cause of cryptogenic cirrhosis.
How Obesity associates with Non-alcoholic Fatty Liver Disease
1, In atudy of "A new risk factor for the development of non-alcoholic fatty liver disease: HLA complex genes" by Celıkbılek M, Selçuk H, Yilmaz U., posted in PubMed, researchers indicated that To reduce the influence of possible confounding factors, we excluded diseases known to be associated with non-alcoholic fatty liver disease like obesity, diabetes mellitus, coronary artery disease, hyperlipidemia, and metabolic syndrome. Non-alcoholic fatty liver disease was diagnosed in 66 individuals (33 male, median age: 53.8 [range, 32-77 years]) by means of ultrasonography data, and 50 individuals, whose ultrasonography data did not show hepatosteatosis, comprised the control group (20 male, median age: 44.6 [range, 26-71 years]). Results: Human leukocyte antigen-B65 (28.8% vs 0%, p<0.001) and DQ5 (40.7% vs 16.1%, p<0.05) were found to be expressed significantly more in non-alcoholic fatty liver disease compared with controls. Serum alanine aminotransferase (27.1 IU/L vs 20 IU/L, p<0.05) was significantly higher in the study group. Conclusions: Our preliminary study suggests that human leukocyte antigen plays a role in the pathogenesis of non-alcoholic fatty liver disease; however, more studies are needed to clarify these data.
2. In a study of "Non-alcoholic steatohepatitis in children" by Nanda K., posted in PubMed, researchers indicated that Obesity has emerged as a significant new health problem in the pediatric population. Non-alcoholic steatohepatitis (NASH),..., A system of grading depending on degree of steatosis and/or inflammation and staging depending on the extent of fibrosis has also been proposed. Although there is no consensus for the treatment for NASH, effort needs to be made to prevent development of fibrosis, which results in cirrhosis and portal hypertension. Slow, consistent weight loss has been shown to be effective in childhood NAFLD, based on improvement of serum aminotransferases or liver sonogram. A low glycemic index diet has been shown to be more effective than a low fat diet in lowering BMI.
3. According to the study of "[Non-alcoholic fatty liver disease--new view]" [Article in Polish], by Raszeja-Wyszomirska J, Lawniczak M, Marlicz W, Miezyńska-Kurtycz J, Milkiewicz P., posted in PubMed, researchers found that The most important therapeutic measure is increasing insulin sensitivity by an attempt to change a lifestyle mostly by dieting and physical activity in order to loose weight. The most used agent is metformin, the others are under controlled trials or their effectiveness is low. NASH is not a common indication for liver transplantation because of the older age distribution of patients and high prevalence of comorbidity, related to metabolic syndrome. Recurence of NASH in the grafted liver is also a relatively frequent complication.
4. In a study of "Serotonin-receptor-3-antagonists improve obesity-associated fatty liver disease in mice" by Haub S, Ritze Y, Ladel I, Saum K, Hubert A, Spruss A, Trautwein C, Bischoff SC., posted in PubMed, researchers found that Palonosetron had similar effects as tropisetron regarding the reduction of liver fat and other parameters. Conclusions: Tropisetron and palonosetron are effective in attenuating NAFLD in a genetic mouse model of obesity. The effect likely involves the intestinal nervous system, resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation.
5. According to the study of "Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis" by Brun P, Castagliuolo I, Di Leo V, Buda A, Pinzani M, Palù G, Martines D., posted in PubMed, researchers found that HSCs isolated from ob/ob and db/db mice showed higher membrane CD14 mRNA levels and more pronounced lipopolysaccharide-induced proinflammatory and fibrogenic responses than HSCs from lean animals. In conclusion, genetically obese mice display enhanced intestinal permeability leading to increased portal endotoxemia that makes HSCs more sensitive to bacterial endotoxins. We suggest that in metabolic syndrome, patients may likewise have a greater intestinal mucosa permeability and increased lipopolysaccharide levels in portal blood that can contribute to the liver inflammatory damage.
6. in the abstract of study of "Animal models of steatohepatitis" by Koteish A, Mae Diehl A., posted in PubMed, researchers indicated that Animal models of hepatic steatosis and steatohepatitis have improved our understanding of the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Three models, genetically obese ob/ob mice, lipoatrophic mice and normal rats fed choline-deficient, methionine-restricted diets, have been particularly informative. All support the multiple 'hit' hypothesis for NAFLD pathogenesis that suggests that fatty livers are unusually vulnerable to oxidants and develop steatohepatitis when secondary insults generate sufficient oxidants to cause liver cell death and inflammation.
7. Etc.
Treatments of Obesity and Non-alcoholic Fatty Liver Disease
1. In a study of"Review article: the metabolic syndrome and non-alcoholic fatty liver disease" by Loria P, Lonardo A, Carulli L, Verrone AM, Ricchi M, Lombardini S, Rudilosso A, Ballestri S, Carulli N., posted in PubMed, researchers stated that Metabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity..... and concluded that Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non-alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance-related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non-alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non-alcoholic fatty liver disease.
2. According to the study of "Non-alcoholic fatty liver disease: further expression of the metabolic syndrome" by Tarantino G, Saldalamacchia G, Conca P, Arena A., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease has been associated with metabolic disorders, including central obesity, dyslipidemia, hypertension and hyperglycemia. Metabolic syndrome, obesity, and insulin resistance are major risk factors in the pathogenesis of non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease refers to a wide spectrum of liver damage, ranging from simple steatosis to non-alcoholic steatohepatitis, advanced fibrosis and cirrhosis.
3. According to the study of "Non-alcoholic steatohepatitis: an overview" by Shifflet A, Wu GY., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of fat-induced liver injury, ranging from mild steatosis to cirrhosis and liver failure. The presence of obesity and insulin resistance is strongly associated with non-alcoholic fatty liver and a greater risk of advanced disease. We present here a review of the mechanisms involved in the pathogenesis of NAFLD, advances in the diagnosis, and options for treatment.
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Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Non-alcoholic Fatty Liver Disease is defined as a condition of the fatty liver diseases as a result of accumulated of fat in the liver, not caused by abusive alcohol consumption. According to the study of "Nonalcoholic Fatty Liver Disease An Underrecognized Cause of Cryptogenic Cirrhosis" by Jeanne M. Clark, MD, MPH, Anna Mae Diehl, MD, posted in The Journals of the American Medical Association, researchers indicated in abstract that Cryptogenic cirrhosis is a common cause of liver-related morbidity and mortality in the United States. Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most common cause of cryptogenic cirrhosis.
How Obesity associates with Non-alcoholic Fatty Liver Disease
1, In atudy of "A new risk factor for the development of non-alcoholic fatty liver disease: HLA complex genes" by Celıkbılek M, Selçuk H, Yilmaz U., posted in PubMed, researchers indicated that To reduce the influence of possible confounding factors, we excluded diseases known to be associated with non-alcoholic fatty liver disease like obesity, diabetes mellitus, coronary artery disease, hyperlipidemia, and metabolic syndrome. Non-alcoholic fatty liver disease was diagnosed in 66 individuals (33 male, median age: 53.8 [range, 32-77 years]) by means of ultrasonography data, and 50 individuals, whose ultrasonography data did not show hepatosteatosis, comprised the control group (20 male, median age: 44.6 [range, 26-71 years]). Results: Human leukocyte antigen-B65 (28.8% vs 0%, p<0.001) and DQ5 (40.7% vs 16.1%, p<0.05) were found to be expressed significantly more in non-alcoholic fatty liver disease compared with controls. Serum alanine aminotransferase (27.1 IU/L vs 20 IU/L, p<0.05) was significantly higher in the study group. Conclusions: Our preliminary study suggests that human leukocyte antigen plays a role in the pathogenesis of non-alcoholic fatty liver disease; however, more studies are needed to clarify these data.
2. In a study of "Non-alcoholic steatohepatitis in children" by Nanda K., posted in PubMed, researchers indicated that Obesity has emerged as a significant new health problem in the pediatric population. Non-alcoholic steatohepatitis (NASH),..., A system of grading depending on degree of steatosis and/or inflammation and staging depending on the extent of fibrosis has also been proposed. Although there is no consensus for the treatment for NASH, effort needs to be made to prevent development of fibrosis, which results in cirrhosis and portal hypertension. Slow, consistent weight loss has been shown to be effective in childhood NAFLD, based on improvement of serum aminotransferases or liver sonogram. A low glycemic index diet has been shown to be more effective than a low fat diet in lowering BMI.
3. According to the study of "[Non-alcoholic fatty liver disease--new view]" [Article in Polish], by Raszeja-Wyszomirska J, Lawniczak M, Marlicz W, Miezyńska-Kurtycz J, Milkiewicz P., posted in PubMed, researchers found that The most important therapeutic measure is increasing insulin sensitivity by an attempt to change a lifestyle mostly by dieting and physical activity in order to loose weight. The most used agent is metformin, the others are under controlled trials or their effectiveness is low. NASH is not a common indication for liver transplantation because of the older age distribution of patients and high prevalence of comorbidity, related to metabolic syndrome. Recurence of NASH in the grafted liver is also a relatively frequent complication.
4. In a study of "Serotonin-receptor-3-antagonists improve obesity-associated fatty liver disease in mice" by Haub S, Ritze Y, Ladel I, Saum K, Hubert A, Spruss A, Trautwein C, Bischoff SC., posted in PubMed, researchers found that Palonosetron had similar effects as tropisetron regarding the reduction of liver fat and other parameters. Conclusions: Tropisetron and palonosetron are effective in attenuating NAFLD in a genetic mouse model of obesity. The effect likely involves the intestinal nervous system, resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation.
5. According to the study of "Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis" by Brun P, Castagliuolo I, Di Leo V, Buda A, Pinzani M, Palù G, Martines D., posted in PubMed, researchers found that HSCs isolated from ob/ob and db/db mice showed higher membrane CD14 mRNA levels and more pronounced lipopolysaccharide-induced proinflammatory and fibrogenic responses than HSCs from lean animals. In conclusion, genetically obese mice display enhanced intestinal permeability leading to increased portal endotoxemia that makes HSCs more sensitive to bacterial endotoxins. We suggest that in metabolic syndrome, patients may likewise have a greater intestinal mucosa permeability and increased lipopolysaccharide levels in portal blood that can contribute to the liver inflammatory damage.
6. in the abstract of study of "Animal models of steatohepatitis" by Koteish A, Mae Diehl A., posted in PubMed, researchers indicated that Animal models of hepatic steatosis and steatohepatitis have improved our understanding of the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Three models, genetically obese ob/ob mice, lipoatrophic mice and normal rats fed choline-deficient, methionine-restricted diets, have been particularly informative. All support the multiple 'hit' hypothesis for NAFLD pathogenesis that suggests that fatty livers are unusually vulnerable to oxidants and develop steatohepatitis when secondary insults generate sufficient oxidants to cause liver cell death and inflammation.
7. Etc.
Treatments of Obesity and Non-alcoholic Fatty Liver Disease
1. In a study of"Review article: the metabolic syndrome and non-alcoholic fatty liver disease" by Loria P, Lonardo A, Carulli L, Verrone AM, Ricchi M, Lombardini S, Rudilosso A, Ballestri S, Carulli N., posted in PubMed, researchers stated that Metabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity..... and concluded that Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non-alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance-related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non-alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non-alcoholic fatty liver disease.
2. According to the study of "Non-alcoholic fatty liver disease: further expression of the metabolic syndrome" by Tarantino G, Saldalamacchia G, Conca P, Arena A., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease has been associated with metabolic disorders, including central obesity, dyslipidemia, hypertension and hyperglycemia. Metabolic syndrome, obesity, and insulin resistance are major risk factors in the pathogenesis of non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease refers to a wide spectrum of liver damage, ranging from simple steatosis to non-alcoholic steatohepatitis, advanced fibrosis and cirrhosis.
3. According to the study of "Non-alcoholic steatohepatitis: an overview" by Shifflet A, Wu GY., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of fat-induced liver injury, ranging from mild steatosis to cirrhosis and liver failure. The presence of obesity and insulin resistance is strongly associated with non-alcoholic fatty liver and a greater risk of advanced disease. We present here a review of the mechanisms involved in the pathogenesis of NAFLD, advances in the diagnosis, and options for treatment.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Super foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
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