Exercise as it relates to Disease/Effect of exercise on adiponectin in improving insulin sensitivity

What is Adiponectin (Ad)?
Adiponectin (Ad) is an adipocyte-derived protein with anti-inflammatory properties and is important for glucose and lipid metabolism. The exact mechanisms involved in the physiological processes of Ad are largely unknown. It is relatively abundant in healthy humans at levels of 2–10 mg/ml. Ad is found in lower concentrations in individuals with: Decreasing adipose tissue has been shown to increase Ad levels. However, individuals with higher adiposity are likely to have increased levels of the Ad receptors, AdipoR1 and AdipoR2, which may be a compensatory mechanism.
 * Coronary artery disease
 * Type 2 diabetes and/or insulin resistance
 * High BMI and/or percentage body fat

The Response of Exercise and Ad in Increasing Insulin Sensitivity
Hypoadiponectinemia is associated with insulin resistance and type 2 diabetes and is a biomarker for assessment of lifestyle changes. Higher levels of Ad have been shown to increase insulin sensitivity through similar mechanisms as the potent effect of exercise muscle contractions in enhancing the insulin-signaling pathway. This is shown in Table 1 and highlights the potential for exercise to enhance the action of Ad when combined.

Table 1: Mechanisms by which Ad and Exercise Increase Insulin Sensitivity

The Impact of Exercise on Ad Secretion
Studies have been conducted on obese, healthy and diabetic individuals and have resulted in disparate conclusions in regards to the effect of exercise on Ad in improving inulin sensitivity. Studies report increases, decreases and no change in Ad levels in response to various acute and chronic exercise programs. This is displayed in Table 2.

Table 2: Effect of Different Exercise on Ad Secretion Increases in Ad levels may be explained by: No change in Ad levels may be explained by: Numerous studies show increases in insulin sensitivity without exhibiting increases in Ad levels, indicating that improvements in insulin sensitivity are not dependent on increases in Ad levels. This suggests that there are other mechanisms involved. One such proposal is an up-regulation of the Ad receptors, AdipoR1 and AdipoR2, in response to exercise.
 * A reduction in body fat,    which could account for the increase rather than adaptive measures to exercise.
 * Adipocytes preforming stores of Ad, which are released in response to exercise.
 * Increases of beta-adrenergic, glucocorticoid, insulin, interleukin-6 and catecholamine activity that is associated with moderate to intense exercise which may impede Ad and Ad gene expression.   This could be a protective mechanism to avoid excessive decreases in glycemia from exercise.

Up-regulation of Ad Receptors
An up-regulation of Ad receptor density in the muscle, more specifically AdipoR1, through acute and chronic exercise increases insulin sensitivity without the requirement of an increase in Ad levels. This achieves the targeted mechanisms and may explain the contradicting findings of the previous section.

Recommendations
There are two known approaches towards increasing the affect of Ad on insulin sensitivity through exercise:
 * 1) Exercise that is favourable for body fat loss is shown to naturally increase Ad secretion.  Aerobic/endurance steady state exercise combined with reduced calorie intake would be sufficient.
 * 2) Acute intensive training and general chronic exercise is shown to increase Ad receptor expression.

Further Resources

 * Diabetes Care Journa- Exercise Increases Adiponectin and Insulin Sensitivity & Insulin Resistance by Adiponectin Deficiency: Is the Action in Skeletal Muscle?
 * Adiponectin and Adiponectin Receptors in Insulin Resistance, Diabetes, and the Metabolic Syndrome
 * Adiponectin: A Fat Cell Hormone that Promotes Insulin Sensitivity