Tuesday, November 07, 2006

Leptin: How Diabetes and Obesity Are Linked

Like two peas in a pod, the obesity and type 2 diabetes epidemics have joined forces in an attempt to ravage America's health ... and it's working, as hundreds of millions of people have been significantly affected by this deadly pair.

But how are these two epidemics intertwined?

Popular belief is that if one eats too much sugar, they'll get fat and develop diabetes; and, if they don't get diabetes it's merely because their body is producing enough insulin to keep up with the sugar. However, researchers have discovered evidence that there's more to the obesity-diabetes connection than this classic way of thinking: The missing link? Leptin.

Mice Studies Shed Light on the Subject
Research on mice has suggested that leptin is the key, as it regulates blood sugar through two different brain-body passageways:
  • One: Responsible for controlling appetite and fat storage
  • Two: Responsible for telling the liver what to do with its stored glucose

While it was previously found that disrupting the appetite-controlling passageway leads to obesity (which significantly increases the risk of diabetes), results of the study indicated that it likely takes disruptions in both of leptin's passageways to trigger full-blown diabetes.

Mice used in the study were genetically modified to disable what is known as the leptin-STAT3 cell-signaling passageway that leads from the brain to the body.

This s/s strain of mice was still able to produce leptin and the receptor it attaches to when sending STAT3 signals in the body.

Further, after eating too much and becoming obese, s/s mice did not develop diabetes; however, other strains of mice that did not produce leptin or have receptors became obese, developed diabetes and died.

Therefore, even when disrupting the leptin-STAT3 signal, the s/s mice were still able to keep their glucose under control, suggesting the likelihood of a brain-liver signaling passageway responsible for regulating blood sugar.

Cell Metabolism March 2005; Vol 1, 169-178 (Free Full-Text Article)
Newswise Mar 16, 2005

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