Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K. et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nat. Med. 7, 941-946
Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Nature Medicine
(Impact Factor: 27.36).
09/2001; 7(8):941-6. DOI: 10.1038/90984
Adiponectin is an adipocyte-derived hormone. Recent genome-wide scans have mapped a susceptibility locus for type 2 diabetes and metabolic syndrome to chromosome 3q27, where the gene encoding adiponectin is located. Here we show that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. Adiponectin decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice. This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin and leptin, but only partially by either adiponectin or leptin alone. We conclude that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy. These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes.
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Available from: Karol Szeszko
- "It plays a dominant role in lipid and carbohydrate metabolism by stimulating fatty acid oxidation, decreasing plasma triglycerides, and increasing cells' sensitivity to insulin and has direct antiatherosclerotic effects (Kadowaki and Yamauchi 2005). Adiponectin is also involved in the regulation of energy balance and body weight and additionally plays a modulatory role in the regulation of the reproductive system (Yamauchi et al. 2001; Kiezun et al. 2014; Maleszka et al. 2014a). "
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ABSTRACT: Reproductive functions are closely related to nutritional status. Recent studies suggest that adiponectin may be a hormonal link between them. Adiponectin is an adipocytokine, abundantly expressed in adipose tissues. It plays a dominant role in lipid and carbohydrate metabolism by stimulating fatty acid oxidation, decreasing plasma triglycerides, and increasing cells' sensitivity to insulin and has direct antiatherosclerotic effects. The hormone is also postulated to play a modulatory role in the regulation of the reproductive system. The aim of this study was to identify differentially expressed genes (DE-genes) in response to adiponectin treatment of porcine luteal ovarian cells. The global expression of genes in the porcine ovary was investigated using the Porcine (V2) Two-color gene expression microarray, 4 × 44 (Agilent, USA). Analysis of the microarray data showed that 701 genes were differentially expressed and 389 genes showed a fold change greater than 1.2 (p < 0.05). Among this number, 186 genes were up-regulated and 203 were down-regulated. The list of DE-genes was used for gene ontology analyses. The biological process list was generated from up-regulated and down-regulated DE-genes. We found that up-regulated products of DE-genes take part in 30 biological processes and down-regulated products in 9. Analysis of the interaction network among DE-genes showed that adiponectin interacts with genes involved in important processes in luteal cells. These results provide a basis for future work describing the detailed interactions and relationships explaining local regulation of adiponectin actions in the ovary of pigs.
Available from: Giuseppe Pizzolanti
- "Data on adiponectin levels in acromegalic patients are very controversial . Adiponectin is an insulin-sensitizing adipokine expressed in human adipose cells with anti-atherogenic and anti-inflammatory properties that plays a role in the pathophysiology of insulin resistance and metabolic syndrome   . Both a condition of hypoadiponectinemia and increased levels of adiponectin in acromegalic patients compared to control subjects have been demonstrated  . "
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ABSTRACT: The studies that have extensively evaluated the relation between adipokines and metabolic parameters in acromegaly treatment are quite discordant. We aimed to evaluate and correlate a set of selected adipokines, known to have a metabolic role, with the disease activity, metabolic status and treatment modalities.
Data of 56 consecutive acromegalic patients (31 M and 25 F; aged 54±12years), admitted to the section of Endocrinology of the University of Palermo during the years 2005-2014, including 16 newly diagnosed untreated (ND), 21 during therapy with somatostatin analogues (SA), 12 with pegvisomant (PE) and 7 after surgical treatment (SU), grouped into uncontrolled (group A: No. 33) and controlled (group B: No. 23) were evaluated. Anthropometric and metabolic parameters, insulin sensitivity indexes, visceral adiposity index (VAI), leptin, soluble leptin receptor, adiponectin, visfatin, resistin, adipsin and non-esterified fatty acids (NEFAs) were assessed. In a subgroup of 21 subjects, the insulin sensitivity index (M value) derived from euglycemic clamp was calculated.
Group A showed higher Homa-IR (p<0.001), VAI (p<0.001), triglycerides (p<0.001), visfatin (p<0.001), and NEFAs (p<0.001) and lower ISI Matsuda (p<0.001), M value (p<0.001), HDL cholesterol (p<0.001) and leptin (p<0.001) than group B. ND patients showed higher VAI, triglycerides, Homa-IR, and visfatin and lower ISI Matsuda, M-value, and leptin compared to other groups (all p<0.050), while no differences were found among SA, PE and SU patients. IGF-1 (p=0.048), M-value (p=0.0029) and VAI (p=0.010) were independently associated with visfatin, while only ISI Matsuda (p=0.019) was associated with leptin.
In acromegaly visfatin could be considered a useful index of disease activity and metabolic alterations, such as insulin resistance and adipose dysfunction, regardless of the type of treatment.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Available from: İsmail Ün
- "Adiponectin is abundantly present in human plasma, the level of which is reduced in obesity, diabetes mellitus and insulin resistance . Furthermore, the adipokine could increase insulin sensitivity . In the present study, 17b-estradiol but not progesterone dramatically suppressed the level of adiponectin, which seems to be in the line of the resistin finding because the decrease in adiponectin concentration could be associated with insulin resistance and other related disorders . "
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ABSTRACT: Effect of female sex hormones on the production/release of adipocyte-derived cytokines has been debatable. Furthermore, whether the cellular signaling triggered by these hormones involve Rho-kinase has not been investigated yet. Therefore, in this study, effects of 17β-estradiol and progesterone as well as the Rho-kinase inhibitor, Y-27632 on the level of adipokines such as resistin, adiponectin, leptin, TNF-α and IL-6 were investigated in 3T3-L1-derived adipocytes. Differentiation was induced in the post-confluent preadipocytes by the standard differentiation medium (Dulbecco's modified Eagle's medium with 10% fetal bovine serum together with the mixture of isobutylmethylxanthine, dexamethasone and insulin) in the presence of 17β-estradiol (10-8-10-7M), progesterone (10-6-10-5M), the Rho-kinase inhibitor, Y-27632 (10-5M) and their combination for 8days. Measurements of the adipokines were performed in the culturing medium by ELISA kits using specific monoclonal antibodies. 17β-estradiol elevated resistin but decreased adiponectin and IL-6 levels; however, it did not alter the concentration of leptin and TNF-α. Y-27632 pretreatment inhibited the rise of resistin and the fall of adiponectin by 17β-estradiol without any effects by its own. Progesterone did not change resistin, leptin and TNF-α level; however, it elevated adiponectin and decreased IL-6 production. Neither 17β-estradiol nor Y-27632 was able to antagonize the increase of adiponectin and the reduction of IL-6 levels by progesterone. While Y-27632 alone lowered IL-6 level, it increased leptin and TNF-α concentration without altering resistin and adiponectin. In conclusion, 17β-estradiol could modify adipokine production in 3T3-L1 adipocytes with the actions some of which involve Rho-kinase mediation.
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