Metabolic Disease And Diabetes

Main Category: Diabetes
Also Included In: Genetics;  Endocrinology
Article Date: 10 May 2011 - 2:00 PDT


Humans with rare genetic mutation point diabetes researchers in the right direction

The cells in the body of an individual with type 2 diabetes are resistant to the effects of the hormone insulin. A few individuals are born resistant to the effects of insulin as a result of mutations in their INSR gene, which templates the protein via which insulin mediates its effects. These individuals provide the unique opportunity to understand the relationship between features of type 2 diabetes and insulin resistance; that is, whether the insulin resistance or the given feature came first). For example, a longstanding question amongst diabetes researchers is whether mitochondrial dysfunction (i.e., dysfunction of the compartments of a cell that generate its energy) causes insulin resistance or vice versa. By studying individuals with INSR mutations, a team of researchers, led by David Savage, at the University of Cambridge, United Kingdom, have now answered this question: defects in insulin signaling can cause dysfunctional mitochondria (at least in these individuals). The team therefore concludes that it is likely that insulin resistance in individuals with type 2 diabetes can impair mitochondrial function.

TITLE: Mitochondrial dysfunction in patients with primary congenital insulin resistance

Clearing the wood from the trees on the function of growth hormone receptor on pancreatic beta-cells

Prior to an individual developing type 2 diabetes, the cells in their body stop responding efficiently to the hormone insulin (i.e., become insulin resistant). This causes a rise in the levels of the energy source glucose in the blood. This, in turn, acts on the insulin-producing cells of the body (pancreatic beta cells) causing them to increase in size and number so that more insulin is produced. Eventually insulin resistance overwhelms the ability of beta-cells to compensate in this way, and the individual becomes diabetic. A team of researchers, led by Derek LeRoith and Shoshana Yakar, at Mount Sinai School of Medicine, New York, has now determined that, in mice, beta-cell expression of the molecule to which growth hormone binds is important if the cells are to increase in number to compensate for conditions that promote type 2 diabetes. Expression of this molecule was also found to be important for glucose stimulation of insulin production. These data help dispel the controversy surrounding the function of growth hormone receptor on beta-cells by providing clear insight into its role on these cells.

TITLE: Growth hormone receptor regulates beta-cell hyperplasia and glucose-stimulated insulin secretion in obese mice

Source:
Karen Honey
Journal of Clinical Investigation

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