Xenical Research Today is a free monthly online journal that collates and summarizes the latest research about Xenical, including details on orlistat, side-effects, obesity, weight loss, dieting. | ||||||||
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{beta}-Cell Lipases and Insulin Secretion.Fex M, Lucas S, Winzell MS, Ahrén B, Holm C, Mulder H Department of Experimental Medical Science, Division of Diabetes, Metabolism, and Endocrinology, Unit of Molecular Metabolism, BMC B11, SE-221 84, Lund, Sweden. hindrik.mulder@med.lu.se. Lipids have been implicated in beta-cell stimulus-secretion coupling. Thus, lipases in beta-cells would be required to generate coupling factors from intracellular lipids. Indeed, we found that glucose stimulates lipolysis in rodent islets and clonal beta-cells. Lipolysis and diglyceride lipase activity in islets are abolished by orlistat, a pan-lipase inhibitor. Moreover, orlistat dose-dependently inhibits glucose- and forskolin-stimulated insulin secretion, while leaving glucose oxidation and the rise in ATP-to-ADP ratio intact. In an effort to identify beta-cell lipase(s), we found that hormone-sensitive lipase (HSL), the rate-limiting enzyme for acylglyceride hydrolysis in adipocytes, is active in rodent beta-cells. To further address the role of HSL, a global and beta-cell-specific inactivation, respectively, of the lipase has been created in mice. Whereas our line of HSL null mice is moderately glucose intolerant due to reduced peripheral insulin sensitivity, it exhibits normal islet metabolism and insulin secretion. Preliminary analysis of the beta-cell-specific HSL knockout has revealed no evidence for disturbed islet function. Thus, studies of ours and others indicate that there is a complex lipid regulatory component in beta-cell stimulus-secretion coupling. The role of HSL and other lipases needs to be further clarified to provide a balanced view of the role of lipids and lipolysis in beta-cells. Published 28 November 2006 in Diabetes, 55: S24-31.
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