SeX(X)Y genes: Unraveling the molecular pathogenesis of disorders of sex development.

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Qualis debeat esse abbas? : de evolutie van abbatiale (zelf-)representaties in Vlaanderen en Lotharingen (ca. 919-1125)

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The logic of the database : in search of responsive social work

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Advanced process control practices for continuous pharmaceutical twin-screw wet granulation

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Lower insulin sensitivity is related to lower relative muscle cross-sectional area, lower muscle density and lower handgrip force in young and middle aged non-diabetic men

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Erchen Decoction and Linguizhugan Decoction Ameliorate Hepatic Insulin Resistance by Inhibiting IRS-1Ser307 Phosphorylation In Vivo and In Vitro

Erchen decoction (ECD) and Linguizhugan decoction (LGZGD), both are Chinese herbal formula, have been used clinically for the treatment of nonalcoholic fatty liver disease (NAFLD). However, their therapeutic mechanisms are still unclear. Because insulin resistance (IR) is a key etiological factor in the pathology of high-fat diet- (HFD-) induced NAFLD, in this study, the protective effects of ECD and LGZGD on HFD-induced insulin resistance in rats were evaluated and their mechanisms were investigated by OGTT and Western blot. The results showed that treatment with ECD and LGZGD significantly improved insulin resistance and liver damage in rats, evidenced by supported serum aminotransferase levels and the histopathological examination. ECD and LGZGD also showed significant protective effects against HFD-induced hyperlipidemia and the inhibition of the hepatocyte proliferation by palmitate. Furthermore, supplementation of ECD and LGZGD decreased TNF-α, NF-κB, and IRS-1Ser307 phosphorylation expressions in vivo and in vitro. These results indicated that ECD and LGZGD have protective effects against HFD-induced liver IR and their underlying mechanisms involve the TNF-α and insulin pathway. These findings would be beneficial for understanding of the therapeutic effects of ECD and LGZGD in treatment of NAFLD.

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Promotion of endocytosis efficiency through an ATP-independent mechanism at rat calyx of held terminals

Abstract

Neurotransmission relies on membrane endocytosis to maintain vesicle supply and membrane stability. Endocytosis has been generally recognized as a major ATP-dependent function, which efficiently retrieves more membrane at elevated neuronal activity when ATP consumption within nerve terminals drastically increases. This paradox raises an interesting question whether increased activity recruits ATP-independent mechanism(s) to accelerate endocytosis while preserving ATP availability for other tasks. To address this issue, we studied ATP requirement in three typical forms of endocytosis at the rat calyx of Held terminals by whole-cell membrane capacitance measurements. At room temperature, blocking ATP hydrolysis effectively abolished slow endocytosis and rapid endocytosis, but only partially inhibited excess endocytosis following intense stimulation. The ATP-independent endocytosis occurred at calyces from postnatal 8–15 days, suggesting its existence before and after hearing onset. This endocytosis was not affected by reduction of exocytosis using the light chain of botulinum toxin C, or by block of clathrin-coat maturation. It was abolished by EGTA, which preferentially blocked endocytosis of retrievable membrane pre-existing at surface, and impaired by oxidation of cholesterol and inhibition of neutral sphingomyelinase. ATP-independent endocytosis became more significant at 34–35°C, and recovered membrane by an amount that on average was close to exocytosis. Our results suggest that activity and temperature recruit ATP-independent endocytosis of pre-existing membrane, in addition to ATP-dependent endocytosis, to efficiently retrieve membrane at nerve terminals. This less understood endocytosis represents a non-canonical mechanism regulated by lipids such as cholesterol and sphingomyelinase.

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