Adipokines: the missing link between insulin resistance and obesity. Diabetes Metab

Inserm U680, faculté de médecine Saint-Antoine, université Pierre-et-Marie-Curie-Paris-6, 75012 Paris, France.
Diabetes & Metabolism (Impact Factor: 2.85). 03/2008; 34(1):2-11. DOI: 10.1016/j.diabet.2007.09.004
Source: PubMed

ABSTRACT White adipose tissue was believed to be just an energy-storage organ, but it is now recognized to be an active participant in energy homoeostasis and physiological functions such as immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Adipose tissue is known to express and secrete a variety of products known as 'adipokines', including leptin, adiponectin, resistin and visfatin, as well as cytokines and chemokines such as tumor necrosis factor-alpha, interleukin-6 and monocyte chemoattractant protein-1. The release of adipokines by either adipocytes or adipose tissue-infiltrated macrophages leads to a chronic subinflammatory state that could play a central role in the development of insulin resistance and type 2 diabetes, and the increased risk of cardiovascular disease associated with obesity.

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    • "In the last decade, several studies have shown elevated IL- 6, TNF, and IL-1 levels in obese patients [13] [14] [15] [16] [17]; however, data regarding the relevance of these cytokines are controversial "
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    ABSTRACT: Obesity is characterized by chronic low-grade inflammation and serves as a major risk factor for hypertension, coronary artery disease, dyslipidemias, and type-2 diabetes. The purpose of this study was to examine changes in metabolic hormones, inflammatory cytokines, and immune function, in lean, overweight, and obese chimpanzees in a controlled environment. We observed increased plasma circulating levels of proinflammatory TH-1 cytokines, Interferon gamma, interleukin-6, interleukin-12p40, tumor necrosis factor, soluble CD40 ligand, and Interleukin-1β and anti-inflammatory TH-2 cytokines, Interleukin-4, Interleukin-RA, Interleukin-10, and Interleukin-13 in overweight and obese chimpanzees. We also observed increased levels of metabolic hormones glucagon-like-peptide-1, glucagon, connecting peptide, insulin, pancreatic peptide YY3-36, and leptin in the plasma of overweight and obese chimpanzees. Chemokine, eotaxin, fractalkine, and monocyte chemoattractant protein-1 were higher in lean compared to obese chimpanzees, while chemokine ligand 8 increased in plasma of obese chimpanzees. We also observed an obesity-related effect on immune function as demonstrated by lower mitogen induced proliferation, and natural killer activity and higher production of IFN-γ by PBMC in Elispot assay, These findings suggest that lean, overweight, and obese chimpanzees share circulating inflammatory cytokines and metabolic hormone levels with humans and that chimpanzees can serve as a useful animal model for human studies.
    09/2014; 2014:856749. DOI:10.1155/2014/856749
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    • "Ovarian exhaustion during the menopausal transition produces endocrine and metabolic changes that relate to body composition and lifestyle habits, stress, and psychosocial adjustments, all which increase weight and the prevalence of the metabolic syndrome (METS). The adipose tissue is a complex and highly active endocrine organ engaging with multiple functions mainly nutrient homeostasis , energy storage, body insulation, thermogenesis, lipid oxidation, adipokine secretion and anti-atherogenesis [1] [2] [3]. Visceral and subcutaneous fat produce a large array of adipokines which display actions on the immune system, endothelium and cardiovascular system, metabolism and inflammation [3] [4] [5] [6]. "
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    ABSTRACT: Objective To measure serum levels of adipsin, leptin, resistin, adiponectin, visfatin, ghrelin and insulin in postmenopausal women screened for the metabolic syndrome (METS). Methods Serum of 100 postmenopausal women was analyzed using multiplex technology for the mentioned analytes. In addition, values for the homeostasis model assessment of insulin resistance (HOMA-IR) were calculated. Comparisons were performed in accordance to the presence or not of the METS and each of its components. Criteria of the American Heart Association were used to define the METS. Results Age and time since menopause onset were similar in women with the METS (n = 57) as compared to those without the syndrome (n = 43). METS women displayed significantly higher levels of adipsin, leptin, resistin, insulin and HOMA-IR values and lower adiponectin levels. These differences were mainly observed among women with abdominal obesity, independent of fulfilling METS criteria or not. In this same sense, lower adiponectin levels significantly related to low HDL-C and high triglyceride levels; and higher insulin and HOMA-IR values related to high triglyceride and glucose levels, respectively. Conclusion In this sample, postmenopausal women with the METS displayed higher insulin and adipokine levels. These were mainly related to abdominal obesity and metabolic and lipid abnormalities. More research is warranted in this regard.
    Maturitas 09/2014; 79(1). DOI:10.1016/j.maturitas.2014.06.008 · 2.86 Impact Factor
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    • "an important inflammatory component is also present in both conditions [7] [8] [9] [10]. Multiple reports have established an association of the immune response and its genetic component with the pathogenesis of ischemic heart disease [11] [12] [13]. "
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    ABSTRACT: Immunologic and inflammatory processes are involved in the pathogenesis of acute coronary syndrome (ACS) and type 2 diabetes mellitus (DM2). Human leukocyte antigen-G (HLA-G) is a negative regulator of the immune response. This study evaluates the 14 bp Del/Ins HLA-G polymorphism in ACS and DM2. Three hundred and seventy individuals from Western Mexico were recruited and categorized into three groups: ACS (86), DM2 without coronary complications (70), and healthy subjects (214). Genotyping of the 14 bp Del/Ins HLA-G polymorphism was performed by PCR and Native-PAGE. The most common risk factors were hypertension and overweight in ACS and DM2, respectively. The genetic distribution of the 14 bp Del/Ins HLA-G polymorphism showed no significant differences between groups (P ≥ 0.23). Nonetheless, the Ins/Ins genotype was associated with high blood pressure (HBP) in the DM2 group (ORc = 1.65, P = 0.02). The genetic recessive model showed similar findings (ORc = 3.03, P = 0.04). No association was found in ACS, with a P of 0.05; nevertheless, the prevalence of Ins/Ins carriers was quite similar to that found in the DM2-HBP group. The 14 bp Del/Ins HLA-G polymorphism was not a susceptibility factor for ACS or DM2; however, the Ins/Ins genotype might have contributed to the development of HBP in the studied groups.
    BioMed Research International 02/2014; 2014:898159. DOI:10.1155/2014/898159 · 2.71 Impact Factor
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