Obesity and Insulin Resistance

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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