The relationship between obesity and diabetes has intrigued scientists for ages. While research corroborated a definitive link between obesity and diabetes, the exact reason between obesity and diabetes is still being understood. A study conducted by researchers at the University of Michigan and Harvard University report new evidence in mice that may help explain that link — and may help them understand why some obese people never develop diabetes while many others do.
In the present study led by senior author Martin G. Myers, Jr., M.D., Ph.D., of the U-M Medical School, researchers genetically modified mice to disable the leptin-STAT3 cell-signalling pathway that leads from the brain to the body. These mice, also called s/s strain mice, were capable of producing both leptin and the receptor it binds to when sending STAT3 signals to the body. The results showed that overeating s/s strain mice did not develop diabetes even after six months, a long time for a mouse. Meanwhile, other strains of mice that made no leptin, or lacked leptin receptors, all became obese and died of diabetes.
Scientists found that a leptin dose of 12.5 ng/hr significantly lowers blood glucose and that 25 ng/hr of leptin normalizes plasma glucose and insulin without significantly reducing body weight, establishing that leptin exerts its most potent effects on glucose metabolism.
These new set of conditions showcased leptin’s antidiabetic effects independent of its ability to correct weight and food intake. This is attributed to a leptin-regulated gene-IGFBP2 in the liver whose expression correlates with leptin’s antidiabetic effect. With more research, scientists hope that these findings can be extended to human clinical settings as well, and develop leptin as a potent anti diabetic treatment.
Article by Snigdha Taduri for Biomed-ME