multiple endocrine neoplasia/triglyceride

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Patients with MEN-1 are more insulin-resistant than their non-affected relatives.

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BACKGROUND Given the clinical impression that patients with type 1 multiple endocrine neoplasia (MEN-1) frequently display abnormal glucose and lipoprotein concentrations, we compared affected subjects followed in our outpatient clinic with their non-affected relatives. METHODS The clinical

Menin prevents liver steatosis through co-activation of peroxisome proliferator-activated receptor alpha.

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Fatty liver is strongly associated with metabolic syndrome. Here, we show that the impaired hepatic expression of menin, the product of the MEN1 (multiple endocrine neoplasia type 1) tumor suppressor gene, represents a common feature of several fatty liver mouse models. The liver specific ablation

Obesity in MENX Rats Is Accompanied by High Circulating Levels of Ghrelin and Improved Insulin Sensitivity.

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Ghrelin, the natural ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a), is mainly secreted from the stomach and regulates food intake and energy homeostasis. p27 regulates cell cycle progression in many cell types. Here, we report that rats affected by the multiple endocrine

Menin liver-specific hemizygous mice challenged with high fat diet show increased weight gain and markers of metabolic impairment.

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OBJECTIVE The menin tumor suppressor protein is abundantly expressed in the liver, although no function has been identified because of lack of tumor development in multiple endocrine neoplasia type 1 (Men1) null livers. We examine the phenotype of mice lacking one functional allele of Men1

Hepatic menin recruits SIRT1 to control liver steatosis through histone deacetylation.

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OBJECTIVE The development and progression of non-alcoholic fatty liver disease are associated with aging, obesity, and type 2 diabetes. Understanding the precise regulatory networks of this process will contribute to novel therapeutic strategies. METHODS Hepatocyte-specific Men1 knockout mice were

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