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Clues to curbing obesity found in neuronal 'sweet spot'

Date:
August 1, 2014
Source:
Yale University
Summary:
Preventing weight gain, obesity, and ultimately diabetes could be as simple as keeping a nuclear receptor from being activated in a small part of the brain, according to a new study.

Preventing weight gain, obesity, and ultimately diabetes could be as simple as keeping a nuclear receptor from being activated in a small part of the brain, according to a new study by Yale School of Medicine researchers.
Credit: Illustration by Patrick Lynch

Preventing weight gain, obesity, and ultimately diabetes could be as simple as keeping a nuclear receptor from being activated in a small part of the brain, according to a new study by Yale School of Medicine researchers.

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Published in the Aug. 1 issue of The Journal of Clinical Investigation (JCI), the study showed that when the researchers blocked the effects of the nuclear receptor PPARgamma in a small number of brain cells in mice, the animals ate less and became resistant to a high-fat diet.

"These animals ate fat and sugar, and did not gain weight, while their control littermates did," said lead author Sabrina Diano, professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine. "We showed that the PPARgamma receptor in neurons that produce POMC could control responses to a high-fat diet without resulting in obesity."

POMC neurons are found in the hypothalamus and regulate food intake. They are the neurons that when activated make you feel full and curb appetite. PPARgamma regulates the activation of these neurons.

Diano and her team studied transgenic mice that were genetically engineered to delete the PPARgamma receptor from POMC neurons. They wanted to see if they could prevent the obesity associated with a high-fat, high-sugar diet.

"When we blocked PPARgamma in these hypothalamic cells, we found an increased level of free radical formation in POMC neurons, and they were more active," said Diano, who is also professor of comparative medicine and neurobiology at Yale and director of the Reproductive Neurosciences Group.

The findings also have key implications in diabetes. PPARgamma is a target of thiazolidinedione (TZD), a class of drugs used to treat type 2 diabetes. They lower blood-glucose levels, however, patients gain weight on these medications.

"Our study suggests that the increased weight gain in diabetic patients treated with TZD could be due to the effect of this drug in the brain, therefore, targeting peripheral PPARgamma to treat type 2 diabetes should be done by developing TZD compounds that can't penetrate the brain," said Diano. "We could keep the benefits of TZD without the side-effects of weight gain. Our next steps in this research are to test this theory in diabetes mouse models."

Other Yale authors on the study included Lihong Long, Chitoku Toda, Jin Kwon Jeong, and Tamas Horvath.

The study was funded by the National Institutes of Health (RO1DK097566)


Story Source:

The above story is based on materials provided by Yale University. The original article was written by Karen N. Peart. Note: Materials may be edited for content and length.


Journal Reference:

  1. Lihong Long, Chitoku Toda, Jing Kwon Jeong, Tamas L. Horvath, Sabrina Diano. PPARγ ablation sensitizes proopiomelanocortin neurons to leptin during high-fat feeding. Journal of Clinical Investigation, 2014; DOI: 10.1172/JCI76220

Cite This Page:

Yale University. "Clues to curbing obesity found in neuronal 'sweet spot'." ScienceDaily. ScienceDaily, 1 August 2014. <www.sciencedaily.com/releases/2014/08/140801213521.htm>.
Yale University. (2014, August 1). Clues to curbing obesity found in neuronal 'sweet spot'. ScienceDaily. Retrieved January 29, 2015 from www.sciencedaily.com/releases/2014/08/140801213521.htm
Yale University. "Clues to curbing obesity found in neuronal 'sweet spot'." ScienceDaily. www.sciencedaily.com/releases/2014/08/140801213521.htm (accessed January 29, 2015).

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