A University of Toledo researcher’s study on how the brain controls weight gain and regulates blood glucose levels appears in the April 7 edition of the journal Cell Metabolism.
Jennifer Hill, assistant professor in the Department of Physiology and Pharmacology and member of the Center for Diabetes and Endocrine Research, eliminated leptin and insulin receptors in brain cells that produce the neuropeptide POMC in mice. POMC neurons are known to suppress feeding in mice and humans.
Prior studies had shown that getting rid of only the receptors for leptin, a circulating protein produced by fat cells, resulted in only a moderate weight gain. That led Hill and her colleagues to speculate that leptin was not the only factor telling POMC neurons how much fat tissue the mice had. Hill then also deleted insulin receptors on POMC neurons. The results were surprising; the double deletion didn’t affect weight. In fact, the mice were a little lighter, but it had a dramatic affect on glucose regulation. Additional testing showed the liver in the mice produce abnormal amounts of glucose.
The finding supports the idea that the hypothalamus communicates with the liver. Without those hormone receptors on POMC neurons, there is no signal to the liver to tell it to stop producing glucose after a meal, Hill said.
The hyperinsulinemia that resulted also had an adverse affect on fertility causing high testosterone levels in females and problems with ovulation.
Hill, who started this study while at the University of Texas Southwestern Medical Center in Dallas, said she hoped the findings would advance the understanding of obesity and fertility.
“We are very pleased the work is published in such a high-profile journal, and my lab is looking forward to conducting follow-up studies,” Hill said.
To see the study, click here.