Associations between alcohol consumption and insulin sensitivity and cardiovascular disease risk factors: the Insulin Resistance and Atherosclerosis Study.

Bell, Ronny A.; Mayer‐Davis, Elizabeth J.; Martin, Michelle; D’Agostino, Ralph B.; Haffner, Steve M.

doi:10.2337/diacare.23.11.1630

Cited by 149 publications

(111 citation statements)

References 44 publications

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“…This finding strongly supports the idea proposed in some human studies of an inverse Ushaped relationship between alcohol intake and insulin sensitivity (12,14,15). However, it is reasonable to assume that at higher alcohol concentrations the inverse U-shaped relationship changes to an inverse J-shaped relationship since other human and animal studies have demonstrated that ethanol consumption can impair insulin-mediated glucose uptake and cause insulin resistance (17)(18)(19).…”

Section: A B C Dsupporting

confidence: 75%

“…Since these controversial observations have not been unraveled to date and the human studies leave some gaps in the complete understanding of the association of light-to-moderate alcohol consumption and insulin sensitivity (15), it was the aim of this study to establish a reliable animal model that will allow more detailed investigations. Male Wistar rats received drinking water without (control) or with different ethanol concentrations (0.5, 1.5, 3, 4.5 and 7%, v/v) for 4 weeks ad libitum.…”

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confidence: 99%

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Low ethanol consumption increases insulin sensitivity in Wistar rats

Furuya

Binsack

Machado

2003

Braz J Med Biol Res

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Several human studies suggest that light-to-moderate alcohol consumption is associated with enhanced insulin sensitivity, but these studies are not free of conflicting results. To determine if ethanolenhanced insulin sensitivity could be demonstrated in an animal model, male Wistar rats were fed a standard chow diet and received drinking water without (control) or with different ethanol concentrations (0.5, 1.5, 3, 4.5 and 7%, v/v) for 4 weeks ad libitum. Then, an intravenous insulin tolerance test (IVITT) was performed to determine insulin sensitivity. Among the ethanol groups, only the 3% ethanol group showed an increase in insulin sensitivity based on the increase of the plasma glucose disappearance rate in the IVITT (30%, P<0.05). In addition, an intravenous glucose tolerance test (IVGTT) was performed in control and 3% ethanol animals. Insulin sensitivity was confirmed in 3% ethanol rats based on the reduction of insulin secretion in the IVGTT (35%, P<0.05), despite the same glucose profile. Additionally, the 3% ethanol treatment did not impair body weight gain or plasma aspartate aminotransferase and alanine aminotransferase activities. Thus, the present study established that 3% ethanol in the drinking water for 4 weeks in normal rats is a model of increased insulin sensitivity, which can be used for further investigations of the mechanisms involved.

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Section: A B C Dsupporting

confidence: 75%

mentioning

confidence: 99%

Low ethanol consumption increases insulin sensitivity in Wistar rats

Furuya

Binsack

Machado

2003

Braz J Med Biol Res

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“…Epidemiological studies suggest that chronic light or heavy ethanol consumption leads to insulin resistance, whereas moderate ethanol consumption results in increased insulin sensitivity [37][38][39][40][41] . In the present study, we found that long-term high-dose ethanol consumption led to insulin resistance in rats, which was consistent with previous studies.…”

Section: Discussionmentioning

confidence: 99%

Long-term ethanol exposure inhibits glucose transporter 4 expression via an AMPK-dependent pathway in adipocytes

Song

Guan

et al. 2010

Acta Pharmacol Sin

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Aim:The roles of AMP-activated protein kinase (AMPK) and myocyte enhancer factor 2 isoforms (MEF2A, D) as mediators of the effects of ethanol on glucose transporter 4 (GLUT4) expression are unclear. We studied the effects of ethanol in adipocytes in vivo and in vitro. Methods: Thirty-six male Wistar rats were divided into three groups and given ethanol in a single daily dose of 0, 0.5, or 5 g/kg for 22 weeks. The expression of AMPK, MEF2 isoforms A and D, and GLUT4 was measured and compared in the three groups. The existence of the AMPK/MEF2/GLUT4 pathway in adipocytes and the effects of ethanol on this pathway were studied in (a) epididymal adipose tissue from six male Wistar rats subcutaneously injected with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR, an AMPK activator) or with 0.9% NaCl (control); and (b) isolated rat and human adipocytes treated with or without ethanol, AICAR, and compound C (a selective AMPK inhibitor). Expression of AMPK, MEF2, and GLUT4 was measured by RT-PCR and Western blotting. Results: (1) Long-term ethanol exposure decreased activated AMPK, MEF2A, MEF2D, and GLUT4 expression in rat adipose tissue. (2) In rat and human adipocytes, AICAR-induced AMPK activation, with subsequent elevation of MEF2 and GLUT4 expression, was inhibited by compound C. (3) In vitro ethanol-treatment suppressed the AMPK/MEF2/GLUT4 pathway. Conclusion: The AMPK/MEF2/GLUT4 pathway exists in both rat and human adipocytes, and activated AMPK may positively regulate MEF2 and GLUT4 expression. Ethanol inhibition of this pathway leads to decreased GLUT4 expression, thus reducing insulin sensitivity and glucose tolerance.

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“…There are biologically plausible explanations for our findings. Among people without diabetes, moderate alcohol consumption may enhance insulin sensitivity [43][44][45][46][47][48][49][50][51] and has been shown to decrease A1C. [52][53][54][55][56] It is plausible that regular, moderate alcohol consumption by people with diabetes similarly enhances insulin sensitivity and improves glycemic control.…”

Section: Discussionmentioning

confidence: 99%