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Obese mice that were genetically engineered to store fat only in fat tissue became very fat indeed, but they did not develop insulin resistance or type 2 diabetes. Why? Because they did not accumulate fat in non-fat tissues such as their liver, heart, or muscles.
The subject mice were altered to produce an excess of adiponectin, a beneficial hormone produced by fat tissue, and a deficiency of leptin, a hormone that suppresses appetite. Adiponectin is usually secreted in an inverse relationship to fat: the fatter one is, the less adiponectin is secreted. In these specially engineered mice, however, adiponectin secretion was high no matter what.
Without the appetite-suppressing action of leptin, the mice overate and became extremely obese. However, they didn't get type 2 diabetes because the adiponectin caused all their extra fat calories to be properly stored in subcutaneous fat tissue instead of in their liver, heart, or muscle tissue.
The researchers report that adiponectin acts as a starvation signal which tells the body that its fat tissue is ready and willing to store more fat. In people who can't appropriately store their fat where it belongs, insulin resistance is the result. The scientists believe that this finding explains why some obese people don't get type 2 diabetes and why some relatively lean people do.
Sources: Medline Plus; Journal of Clinical Investigation, August 2007
1 comment - Oct 16, 2007