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Vitamin D activates the hypothalamus (in rodents) to reduce weight and diabetes– May 2016

Hypothalamic Vitamin D Improves Glucose Homeostasis and Reduces Weight

Diabetes. 2016 May 23. pii: db160309. [Epub ahead of print]
Sisley SR1, Arble DM2, Chambers AP3, Gutierrez-Aguilar R4, He Y5, Xu Y5, Gardner D6, Moore DD7, Seeley RJ2, Sandoval DA2.
1Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030 Stephanie.sisley at bcm.edu.
2Department of Surgery, University of Michigan, Ann Arbor, MI 48105.
3Department of Incretin and Obesity Pharmacology, Novo Nordisk, 2760 MÅLØV, Denmark.
4División de Investigación, Facultad de Medicina, Universidad Nacional Autónoma de México Laboratorio de Enfermedades Metabólicas: Obesidad y Diabetes, Hospital Infantil de México "Federico Gómez", México.
5Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030.
6Diabetes Center, University of California San Francisco, San Francisco, CA 94143.
7Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030.

Despite clear associations between vitamin D deficiency and obesity and/or type 2 diabetes, a causal relationship is not established. Vitamin D receptors (VDR) are found within multiple tissues, including the brain. Given the importance of the brain in controlling both glucose levels and body weight, we hypothesized that activation of central VDR links vitamin D to the regulation of glucose and energy homeostasis. Indeed, we found that small doses of active vitamin D, 1,25D3 (calcitriol), into the third-ventricle of the brain improved glucose tolerance and markedly increased hepatic insulin sensitivity, an effect that is dependent upon VDR within the paraventricular nucleus of the hypothalamus.

In addition, chronic central administration of 1,25D3 dramatically decreased body weight by lowering food intake in obese rodents.

Our data indicate 1,25D3-mediated changes in food intake occurs through action within the arcuate nucleus. We found that VDR co-localized with and activated key appetite regulating neurons in the arcuate, namely pro-opiomelanocortin neurons (POMC). Together, these findings define a novel pathway for vitamin D regulation of metabolism with unique and divergent roles for CNS VDR signaling. Specifically, our data suggest that vitamin D regulates glucose homeostasis via the paraventricular nuclei and energy homeostasis via the arcuate nuclei.

© 2016 by the American Diabetes Association. PMID: 27217488

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