A. 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.
B. How to calculate your BMI index
BMI= weight (kg)/ height (m2)
C. 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.
D. 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.
E. 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.
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