Regulation of adiponectin receptor gene expression in diabetic mice

Inukai, Kouichi; Nakashima, Youhei; Watanabe, Masaki; Takata, Nobuki; Sawa, Takahiro; Kurihara, Susumu; Awata, Takuya; Katayama, Shigehiro

doi:10.1152/ajpendo.00118.2004

Cited by 92 publications

(95 citation statements)

References 33 publications

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“…This was correlated with decreased APN binding to membrane fractions of skeletal muscle, and decreased AMPK activation by APN. Similarly, Inukai and colleagues [72] found that insulin had an inhibitory effect on AdipoR1 expression, in a mechanism mediated by the PI3K-dependent pathway rather than the MAPK pathway. In contrast to Inukai, Staiger and colleagues [73] reported that insulin did not directly modify AdipoR1 mRNA expression in human skeletal muscle cells.…”

Section: Interrelationship Between Insulin Signaling and Apn Signalingmentioning

confidence: 87%

Adiponectin resistance and vascular dysfunction in the hyperlipidemic state

Liang

2010

Acta Pharmacol Sin

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Insulin plays an important role in the stimulation of vascular nitric oxide production, with both short term (vasomotility and antithrombotic effects) and long term (smooth muscle cell growth and migration inhibition) benefits. Impaired vasodilatory response to insulin, the hallmark of vascular insulin resistance (IR), has important implications for circulatory pathophysiology. An association between adipokines and IR has been observed in both diabetic and nondiabetic states. Adiponectin (APN) is an insulin-sensitizing adipokine known to stimulate skeletal muscle fatty acid (FA) oxidation and reduce lipid accumulation. Recent demonstrations of potential cross-talk between APN and insulin in vascular function regulation are particularly interesting. The lipid accumulation observed after chronic high-fat (HF) diets and in the obese state may reduce vascular response to APN, a pathologic state termed as APN resistance. This review highlights the importance of insulin sensitivity and APN activity in the maintenance of endothelial function. It explores the relationships between vascular IR and APN resistance in the hyperlipidemic pathological condition, representative of the metabolic syndrome. The investigation of vascular insulin and APN resistance provides not only better understanding of vascular pathophysiology, but also an opportunity for therapeutic targeting in individuals affected by the metabolic syndrome.

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Section: Interrelationship Between Insulin Signaling and Apn Signalingmentioning

confidence: 87%

Adiponectin resistance and vascular dysfunction in the hyperlipidemic state

Liang

2010

Acta Pharmacol Sin

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“…ADIPOR1 mRNA expression in human skeletal muscle cells was positively correlated with in vivo insulin secretion and plasma lipid concentrations, whereas the expression of ADIPOR2 was not associated with most of these metabolic parameters (9). In addition, it was recently found that regulation of ADIPOR1, rather than ADIPOR2, might be involved in glucose and lipid metabolism in diabetic states (37).…”

Section: Discussionmentioning

confidence: 99%

Variations in Adiponectin Receptor Genes and Susceptibility to Type 2 Diabetes in Women

Doria²,

Giorgi³

et al. 2007

Diabetes

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Adiponectin has been associated with low diabetes risk. The metabolic effects of adiponectin are mediated by adiponectin receptors 1 (ADIPOR1) and 2 (ADIPOR2). We conducted a prospective, nested case-control study of 714 cases of type 2 diabetes and 1,120 control subjects. Six polymorphisms in ADIPOR1 and 16 polymorphisms in ADI-POR2 were determined. Haplotypes inferred from ADI-POR1 polymorphisms were significantly associated with diabetes risk (overall test, ؊2log-likelihood ‫؍‬ 15.1 on 5 df; P ‫؍‬ 0.0098). A single copy of haplotype 001100 (0, common allele; and 1, minor allele) was associated with 24% M any studies have documented that adiponectin, which is a hormonal cytokine secreted exclusively by adipose tissue, has strong insulin-sensitizing, anti-inflammatory, and antidiabetes effects (1,2). Adiponectin improves insulin sensitivity by affecting the metabolism of glucose and lipids in skeletal muscle and liver (3). In earlier analyses, we have found that blood adiponectin levels and variations in the adiponectin gene (ADIPOQ, also known as APM1) were associated with type 2 diabetes and cardiovascular risk (4 -6).Recent evidence indicates that the metabolic regulation of adiponectin is mainly mediated by two types of receptors, adiponectin receptors 1 (ADIPOR1) and 2 (ADI-POR2) (7,8). Downregulation of ADIPORs may blunt adiponectin-induced signaling (7). The expression of adiponectin receptor has been related to in vivo parameters of glucose and lipid metabolism (9) and was found to be lower in diabetic patients (10). The polymorphisms in the ADIPOR1 gene were recently associated with adiposity, insulin resistance, and high liver fat (11-13). A few studies have investigated the associations between the variations in ADIPOR1 and ADIPOR2 genes and the risk of type 2 diabetes but generated mixed results (14 -17). These studies, however, were largely limited by small sample size or a cross-sectional nature in design. The relation between ADIPOR genetic variability and diabetes risk has yet to be evaluated in prospective settings.In this study, we comprehensively examined the variations in ADIPOR1 and ADIPOR2 genes and the risk of type 2 diabetes in a nested, case-control study from the Nurses' Health Study cohort. We selected linkage disequilibrium (LD) tagging single nucleotide polymorphisms (SNPs) that capture the maximum variance in both genes and also included polymorphisms that were previously associated with diabetes risk. RESEARCH DESIGN AND METHODSThe Nurses' Health Study was established in 1976 when 121,700 female registered nurses aged 30 -55 years and residing in 11 large U.S. states completed a mailed questionnaire on medical history and lifestyle (18). The lifestyle factors, including smoking, menopausal status and postmenopausal hormone therapy, and body weight, have been updated by validated questionnaires every 2 years. Samples for the present case-control study were selected from a subcohort of 32,826 women who provided a blood sample between 1989 and 1990 and were free from diabetes, cardio...

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“…0 primer-GACTGTACAAATCACGTTGGGA), and GAPDH (5 0 primer-TTGTCTCCTGCGACTTCA, 3 0 primer-CACCACC-CTGTTGCTGTA) were employed (28)(29)(30)(31). To assess the specificity of each primer set, amplicons generated from the PCR reaction were analyzed for melting curves and also by electrophoresis in 2% agarose gels.…”

Section: Real-time Pcr Analysismentioning

confidence: 99%

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

Teraoka

Mutoh

Takasu

et al. 2011

Cancer Prevention Research

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It has been suggested that hyperlipidemia is positively associated with colon carcinogenesis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors, reduce serum lipid levels. In this study, we clarified the effects of a novel chemically synthesized statin, pitavastatin, on intestinal polyp formation in Min mice, and further examined serum lipid and adipocytokine levels, and proinflammatory and adipocytokine gene levels in intestinal mucosa of Min mice. Treatment with pitavastatin at doses of 20 and 40 ppm decreased the total number of polyps dose-dependently to 85.2% and 65.8% (P < 0.05) of the untreated value, respectively. Serum levels of total cholesterol and triglyceride were slightly reduced and those of IL-6, leptin, and MCP-1 were decreased by 40-ppm pitavastatin treatment. mRNA expression levels of cyclooxygenase-2, IL-6, inducible nitric oxide (iNOS), MCP-1, and Pai-1 were significantly reduced in intestinal nonpolyp parts by pitavastatin treatment. Among them, iNOS mRNA levels were also reduced in the intestinal polyps. Moreover, oxidative stress represented by 8-nitroguanosine in the small intestinal epithelial cells was reduced by pitavastatin treatment. Related to these proinflammatory genes, PPARg activity was activated in the intestinal nonpolyp parts and in the liver of Min mice with pitavastatin treatment. These results indicated that pitavastatin has potential benefit for the suppression of intestinal polyp development. Cancer Prev Res; 4(3); 445-53. Ó2011 AACR.

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Regulation of adiponectin receptor gene expression in diabetic mice

Cited by 92 publications

References 33 publications

Adiponectin resistance and vascular dysfunction in the hyperlipidemic state

Adiponectin resistance and vascular dysfunction in the hyperlipidemic state

Variations in Adiponectin Receptor Genes and Susceptibility to Type 2 Diabetes in Women

Inhibition of Intestinal Polyp Formation by Pitavastatin, a HMG-CoA Reductase Inhibitor

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