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
No comments:
Post a Comment