Abstract
Elevated hepatic glucose production, impaired insulin secretion, and insulin resistance - abnormalities of glucose metabolism typically found in subjects with obesity - are major factors underlying the pathogenesis of type 2 diabetes (DM2) and the metabolic syndrome (MS). Adiponectin is a major regulator of glucose and lipid homeostasis via its insulin-sensitizing properties, and lower levels seems to be associated with the development of DM2 and MS. The purpose of this review is to clarify the mechanisms whereby adiponectin relates to the development of DM2 and MS and the association between polymorphisms of the adiponectin gene, circulating levels of the hormone, and its relationships with DM2. In addition, the impact of dietary lipids in the circulating levels of adiponectin will be addressed. According to the literature, circulating adiponectin levels seem to decrease as the number of MS components increases. Lower adiponectin concentrations are associated with higher intra-abdominal fat content. Therefore, adiponectin could link intra-abdominal fat with insulin resistance and development of MS. Therapeutic strategies that target the MS and its components, such as lifestyle modification through physical activity and weight loss, have been shown to increase adiponectin concentrations. Possible roles of diets containing either low or high amounts of fat, or different types of fat, have been analyzed in several studies, with heterogeneous results. Supplementation with n-3 PUFA modestly increases adiponectin levels, whereas conjugated linoleic acid supplementation appears to reduce concentrations when compared with unsaturated fatty acid supplementation used as an active placebo.
Highlights
The prevalence of the metabolic syndrome (MS) and diabetes mellitus type 2 (DM2) in the North American population is 22.9% and 9.3%, respectively, according to NHANES and CDC data [1,2]
Obesity and abdominal fat deposition cause a number of metabolic abnormalities that result in increased hepatic glucose output and decreased insulin sensitivity in skeletal muscle, liver, and adipose tissue – processes that are closely related to the pathogenesis of DM2 [10]
Providing isocaloric diets for weight maintenance with high fat (55% fat, 27% carbohydrates, 18% protein) or low fat (20% fat, 62% carbohydrates, 18 % protein) was not associated with differences in adiponectin levels after 4 weeks of intervention [74]. These results suggest there is no consensus about the effect of total dietary lipid intake on adiponectin levels in interventional studies conducted in humans
Summary
The prevalence of the metabolic syndrome (MS) and diabetes mellitus type 2 (DM2) in the North American population is 22.9% and 9.3%, respectively, according to NHANES and CDC data [1,2]. In a recent systematic review of cross-sectional studies, the weighted average prevalence of MS was 29.8%, 20.1%, and 41.5% in the adult Brazilian population in urban, rural, and indigenous areas, respectively [3]. Its estimated cost per capita is US$ 1527.6/year; considering that an estimated 11.6 million Brazilians aged 20 to 79 have DM2, direct expenses related to this condition amount to approximately US$ 17 billion a year [8]. Obesity and abdominal fat deposition cause a number of metabolic abnormalities that result in increased hepatic glucose output and decreased insulin sensitivity in skeletal muscle, liver, and adipose tissue – processes that are closely related to the pathogenesis of DM2 [10]. The impact of diets with different levels and types of lipids on circulating levels of adiponectin will be addressed
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