Ethanol influence on insulin secretion from isolated rat islets

Singh, Sant P.; Patel, D. G.; Snyder, Ann K.; Pullen, Gordon L.

doi:10.1007/bf01975895

Cited by 10 publications

(9 citation statements)

References 18 publications

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“…In addition, pancreatic cirrhosis, which sometimes seen in alcoholics, may also hamper insulin secretion from the pancreas. In that the former events do occur at an ethanol concentration of much higher than the physiological level [43], we believe that they were not involved in the present observations. Furthermore, in that this population did not contain subjects suffering from diabetes and chronic alcoholic pancreatitis, two major complications of pancreatic cirrhosis, it is most likely that those who were suffering from severe pancreatic cirrhosis were not included in the present subjects.…”

Section: Resultsmentioning

confidence: 72%

Beneficial Effects of Ethanol Consumption on Insulin Resistance Are Only Applicable to Subjects Without Obesity or Insulin Resistance; Drinking is not Necessarily a Remedy for Metabolic Syndrome

Yokoyama

2011

IJERPH

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Although moderate drinking has been shown to lower insulin resistance levels, it is still unclear whether alcoholic beverages could be remedies for insulin resistance. To elucidate this, the correlation between levels of ethanol consumption and insulin resistance were cross-sectionally examined in 371 non-diabetic male Japanese workers. Multiple regression analysis demonstrated that the ethanol consumption level was inversely correlated with the insulin resistance level assessed by homeostatic model assessment (HOMA-IR, p = 0.0014), the serum insulin level (p = 0.0007), and pancreatic β-cell function, also assessed by HOMA (HOMA-β, p = 0.0002), independently from age, body mass index (BMI), and blood pressure, liver function tests, and lipid profiles status, as well as serum adiponectin. The correlations were true in subjects with normal BMIs (up to 25.0 kg/m2, n = 301) or normal HOMA-IR (up to 2.0 μIU·mg/μL·dL n = 337), whereas all of them were non-significant in those with excessive BMIs (n = 70) or in those with HOMA-IR of more than 2.0 (n = 34). Although it is still unclear whether the reductions of these parameters by ethanol consumption are truly due to the improvement of insulin resistance, at least, these effects are not applicable to subjects with obesity and/or insulin resistance. Thus, alcoholic beverages could not be remedies for insulin resistance or metabolic syndrome.

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Section: Resultsmentioning

confidence: 72%

Beneficial Effects of Ethanol Consumption on Insulin Resistance Are Only Applicable to Subjects Without Obesity or Insulin Resistance; Drinking is not Necessarily a Remedy for Metabolic Syndrome

Yokoyama

2011

IJERPH

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“…In addition, insulin is known to decrease the CYP2E1 content by destabilizing its mRNA (de Waziers et al, 1995; Woodcroft et al, 2002), possibly leading to reduced ROS production from CYP2E1-mediated reactions. However, chronic and binge ethanol exposures promote apoptosis and necroinflammation of pancreatic beta cells resulting in decreased insulin production and secretion (see review by Pandol and Raraty, 2007; Shin et al, 2002; Singh et al, 1986). Chronic and binge ethanol exposure also interrupts the normal insulin signaling pathways in various target organs including the liver, contributing to decreased proliferation of hepatocytes and insulin resistance with fatty liver in animals and humans (de la Monte et al, 2008; He et al, 2007; Kang et al, 2007b; Mohr et al, 1998; Shelmet et al, 1988).…”

Section: J Role Of Insulinmentioning

confidence: 99%

Molecular Mechanisms of Alcoholic Fatty Liver

Purohit

Gao

Song

2009

Alcoholism Clin & Exp Res

279

242

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Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. Alcohol exposure may induce fatty liver by increasing NADH/NAD + ratio, increasing sterol regulatory element-binding protein-1 (SREBP-1) activity, decreasing peroxisome proliferator-activated receptor-α (PPAR-α) activity, and increasing complement C3 hepatic levels. Alcohol may increase SREBP-1 activity by decreasing the activities of AMP-activated protein kinase and sirtuin-1. Tumor necrosis factor-α (TNF-α) produced in response to alcohol exposure may cause fatty liver by up-regulating SREBP-1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down-regulating SREBP-1 activity. PPAR-α agonists have potentials to attenuate alcoholic fatty liver. Adiponectin and interleukin-6 may attenuate alcoholic fatty liver by up-regulating PPAR-α and insulin signaling pathways while down-regulating SREBP-1 activity, and suppressing TNF-α production. Recent studies show that paracrine activation of hepatic cannabinoid receptor 1 by hepatic stellate cell-derived endocannabinoids also contributes to the development of alcoholic fatty liver. Furthermore, oxidative modifications and inactivation of the enzymes involved in the mitochondrial and/or peroxisomal β-oxidation of fatty acids could contribute to fat accumulation in the liver.

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“…Recent studies have found that ethanol increases insulin resistance in liver and skeletal muscle [3–5]. However, a limited number of studies have reported on deleterious effects of ethanol on β‐cells, where ethanol inhibited insulin secretion [6–8]. Excessive ethanol consumption leads to cell injury through the production of reactive oxygen species (ROS) and mitochondrial dysfunction [9,10].…”

Section: Introductionmentioning

confidence: 99%

“…have reported on deleterious effects of ethanol on b-cells, where ethanol inhibited insulin secretion [6][7][8]. Excessive ethanol consumption leads to cell injury through the production of reactive oxygen species (ROS) and mitochondrial dysfunction [9,10].…”

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confidence: 99%

Prohibitin is expressed in pancreatic β‐cells and protects against oxidative and proapoptotic effects of ethanol

et al. 2010

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Pancreatic β‐cell dysfunction is a prerequisite for the development of type 2 diabetes. Alcoholism is a diabetes risk factor and ethanol increases oxidative stress in β‐cells, whereas the mitochondrial chaperone prohibitin (PHB) has antioxidant effects in several cell types. In the present study we investigated whether PHB is expressed in β‐cells and protects these cells against deleterious effects of ethanol, using INS‐1E and RINm5F β‐cell lines. Endogenous PHB was detected by western blot and immunocytochemistry. Reactive oxygen species were determined by 5‐(and‐6)‐chloromethyl‐2′,7′‐dichlorodihydrofluorescein diacetate fluorescence assay, and mitochondrial activity was assessed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide (MTT) reduction, uncoupling protein 2 expression and ATP production. Cell death was determined by Hoechst 33342 staining, cleaved caspase‐3 levels and flow cytometry. PHB was expressed in β‐cells under normal conditions and colocalized with Hoechst 33342 in the nucleus and with the mitochondrial probe Mitofluor in the perinuclear area. In ethanol‐treated cells, MTT reduction and ATP production decreased, whereas reactive oxygen species, uncoupling protein 2 and cleaved caspase‐3 levels increased. In addition, flow cytometry analysis showed an increase of apoptotic cells. Ethanol treatment increased PHB expression and induced PHB translocation from the nucleus to the mitochondria. PHB overexpression decreased the apoptotic effects of ethanol, whereas PHB knockdown enhanced these effects. The protective effects of endogenous PHB were recapitulated by incubation of the cells with recombinant human PHB. Thus, PHB is expressed in β‐cells, increases with oxidative stress and protects the cells against deleterious effects of ethanol.

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Ethanol influence on insulin secretion from isolated rat islets

Cited by 10 publications

References 18 publications

Beneficial Effects of Ethanol Consumption on Insulin Resistance Are Only Applicable to Subjects Without Obesity or Insulin Resistance; Drinking is not Necessarily a Remedy for Metabolic Syndrome

Beneficial Effects of Ethanol Consumption on Insulin Resistance Are Only Applicable to Subjects Without Obesity or Insulin Resistance; Drinking is not Necessarily a Remedy for Metabolic Syndrome

Molecular Mechanisms of Alcoholic Fatty Liver

Prohibitin is expressed in pancreatic β‐cells and protects against oxidative and proapoptotic effects of ethanol

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