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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    • "ApN level and body mass index are inversely correlated. normal weight people have a physiologically increased serum ApN level in contrast, in obese individuals ApN biosynthesis is down regulated, which leads to hypoadiponectinemia, not only BMI, but also the risk for BC is inversely correlated with ApN level in serum [17] [18]. Leptin is an anorexigenic peptide that plays a key role in energy homeostasis and appetite control [19]. "

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    • "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.
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    • "Учитывая полученные данные, терапевтическая и хирургическая коррекция ожирения нормализуют плазменные уровни адипонектина. В то же время, отсутствие положительной динамики уровней адипонектина, резистина и висфатина в зависимости от ИМТ в терапевтической и хирургической группах подтверждает тот факт, что полученные в эксперименте результаты не всегда экстраполируются в клинику[21], и что может свидетельствовать в пользу того, что основные механизмы ауто-и паракринного регуляторного влияния адипокинов на метаболизм осуществляются в пределах ЖТ, путем изменения ее чувствительности к инсулину. На наш взгляд, необходимо определение тканеспецифической экспрессии этих медиаторов клетками ЖТ – адипоцитами. "
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    ABSTRACT: Bariatric surgery serves as a model for the assessment of the relationship between body mass index (BMI) reduction and changes in adipokine production and for exploring the endocrine function of the pancreas in patients who do not have the proximal part of the small intestine. Aim: of the study was to assess the biochemical parameters and plasma levels of adipokines [adiponectin, adipsin, leptin, plasminogen activator inhibitor (PAI-1), resistin and visfatin], insulin, C-peptide, ghrelin and incretins [glucose insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1)] in patients with morbid obesity after surgery (gastric bypass) and therapeutic correction. Materials and methods: A total of 75 patients (34 men and 41 women; age range: 24-67 years) diagnosed as obese were divided into two groups according to the treatment they received. Biochemical analysis was performed to estimate carbohydrate and lipid metabolism rates and plasma levels of adipokines (adiponectin, adipsin, leptin, PAI-1, resistin, visfatin), insulin, C-peptide, ghrelin and incretins (GIP and GLP-1) using the flow fluorometry. Results: Surgical treatment of obesity resulted in a significant decrease in BMI (from 45.67±9.87 to 32.45±5.35 kg/m2, p<0.05). Carbohydrate metabolism parameters and HOMA-IR index independent of BMI were comparable to the reference values after gastric bypass (18 months later). A direct correlation of plasma PAI-1 and leptin levels with BMI in groups with conservative (r=0.800, p=0.004 and r=0.780, p=0.010) and surgical treatment (r=-0.670, p=0.001 and r=0.760, p=0.01) was observed. Elevated leptin levels in patients with morbid obesity after gastric bypass with normal glucose and insulin levels indicated an indirect effect of leptin levels on the development of insulin resistance in metabolic syndrome. Conclusions: Gastric bypass is a more efficient approach to reduce obesity. Adipokine (leptin and PAI-1) production and adipose tissue mass are directly correlated.
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