Adiponectin in insulin resistance: lessons from translational research. Am J Clin Nutr 91:258S-261S

Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 11/2009; 91(1):258S-261S. DOI: 10.3945/ajcn.2009.28449C
Source: PubMed


Adiponectin is an adipose tissue-secreted endogenous insulin sensitizer, which plays a key role as a mediator of peroxisome proliferator-activated receptor gamma action. Adiponectin alters glucose metabolism and insulin sensitivity, exhibits antiinflammatory and antiatherogenic properties, and has been linked to several malignancies. Circulating concentrations of adiponectin are determined primarily by genetic factors, nutrition, exercise, and abdominal adiposity. Adiponectin concentrations are lower in subjects with obesity, metabolic syndrome, and cardiovascular disease. Adiponectin knockout mice manifest glucose intolerance, insulin resistance, and hyperlipidemia and tend to develop malignancies especially when on high-fat diets. Animal studies have also shown beneficial effects of adiponectin in rodents in vivo. Circulating concentrations of adiponectin are lower in patients with diabetes, cardiovascular disease, and several malignancies. Studies to date provide promising results for the diagnostic and therapeutic role of adiponectin in obesity, insulin resistance, diabetes, cardiovascular disease, and obesity-associated malignancies.

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    • "However, the reasons underling the high incidence of MS have not been confirmed. Related studies have demonstrated that MS is associated with a proinflammatory state, which is hypothesized to be related to CVD [20] [21] [22] [23], and some inflammatory markers, such as IL-6, hsCRP, FFA, and adiponectin, are closely related to MS [21] [24] [25]. "
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    ABSTRACT: This study focused on low-income rural and nomadic minority people residing in China's far west and investigated their relationship between inflammatory markers (IL-6, hsCRP, FFA, and adiponectin) and MS and ethnic differences. And it found that improving behavioral lifestyle by education or using drugs to control inflammation may prevent MS. These observations may benefit low-income populations.
    Mediators of Inflammation 08/2015; 2015(10):706768. DOI:10.1155/2015/706768 · 3.24 Impact Factor
    • "Obesity is closely linked to the development of T2DM and the hypertrophic adipocytes secrete peptides that have been implicated in the onset of insulin resistance (Kahn et al., 2006; Hajer et al., 2008). Chronically elevated levels of some saturated fatty acids are also known to be involved in metabolic dysregulation, through decreased production of the insulin sensitising fat-derived hormone adiponectin, reduced insulin-stimulated glucose uptake and increased β-cell death (Kennedy et al., 2009; Kusminski et al., 2009; Ziemke & Mantzoros, 2010). In recent years it has become apparent that adipocytes also secrete phospholipid-derived messengers known as endocannabinoids, which show elevated levels in obesity (Bluher et al., 2006) and may contribute to insulin resistance (Li et al., 2011). "
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    ABSTRACT: GPR55 belongs to the class A family of G-protein coupled receptor (GPCRs) and its activity is regulated by a range of synthetic and endogenous cannabinoids, and by lipid-derived ligands. Cannabinoids are known to be important in controlling appetite and metabolic balance, and it is now emerging that GPR55 may have a role to play in energy homeostasis through the regulation of food intake, fuel storage in adipocytes, gut motility and insulin secretion. This review summarises our current knowledge of expression and function of GPR55 in tissues involved in metabolic regulation, the signalling cascades through which GPR55 is reported to act to exert its effects, and it comments on the difficulties in reaching firm conclusions when using GPR55 ligands of poor specificity. Understanding the role of GPR55 in energy homeostasis may provide a novel target for therapeutic intervention in obesity and type 2 diabetes mellitus.
    Pharmacology [?] Therapeutics 06/2014; 145. DOI:10.1016/j.pharmthera.2014.06.007 · 9.72 Impact Factor
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    • "Insulin resistance is a key component of type 2 diabetes, and is also associated with obesity, especially visceral fat obesity21, hypertension22, dyslipidemia23, and hypoadiponectinemia24. Furthermore, the abnormalities associated with insulin resistance have been suggested to increase the risk of cardiovascular disease3. "
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    ABSTRACT: Aims/IntroductionTo establish the validity of the plasma glucose disappearance rate (KITT), derived from an insulin-tolerance test (ITT), for evaluating the insulin sensitivity of patients with type 2 diabetes after insulin therapy.Materials and Methods In the first arm of the study, 19 patients with poorly controlled diabetes were treated with insulin and underwent an ITT and a euglycemic clamp test (clamp-IR). The relationship between the insulin resistance index, as assessed by both the clamp-IR and KITT tests, was examined. In the second arm of the study, the relationships between KITT values and various clinical parameters were investigated in 135 patients with poorly controlled diabetes, after achieving glycemic control with insulin.ResultsIn study 1, a close correlation between KITT and the average glucose infusion rate during the last 30 min of the standard clamp-IR test (M-value) was noted (P < 0.001). In study 2, body mass index (P = 0.0011), waist circumference (P = 0.0004), visceral fat area (P = 0.0011) and the log-transformed homeostasis model assessment of insulin resistance value (P = 0.0003) were negatively correlated with the log-transformed KITT. High-density lipoprotein cholesterol (P = 0.0183), low-density lipoprotein cholesterol (P = 0.0121) and adiponectin (P = 0.0384) levels were positively correlated with the log-transformed KITT.Conclusions The ITT is a valid and useful test for evaluating the insulin sensitivity of patients with diabetes, even after treatment with insulin.
    05/2014; 5(3). DOI:10.1111/jdi.12143
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