Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 122, Issue 1, Pages 153-162Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI59660
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Funding
- NIH [DK088872, DK068384, DK083042, DK052989, DK077975, DK080000]
- Diabetes Endocrinology Research Center (DERC) [DK017047]
- Netherlands Organization for Scientific Research
- Office of Research and Development, Department of Veterans Affairs
- Nutrition Obesity Research Center [DK035816]
- Mouse Metabolic Phenotyping Center [U24 DK076126]
- Cellular and Molecular Imaging Core of the DERC at the University of Washington [DK017047]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [U24DK076126, P30DK017047, R01DK074758, P01DK068384, R01DK080000, K08DK088872, R01DK052989, R01DK077975, R01DK083042, DP1DK098058, R01DK090320, P30DK035816] Funding Source: NIH RePORTER
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Rodent models of obesity induced by consuming high-fat diet (HFD) are characterized by inflammation both in peripheral tissues and in hypothalamic areas critical for energy homeostasis. Here we report that unlike inflammation in peripheral tissues, which develops as a consequence of obesity, hypothalamic inflammatory signaling was evident in both rats and mice within 1 to 3 days of HFD onset, prior to substantial weight gain. Furthermore, both reactive gliosis and markers suggestive of neuron injury were evident in the hypothalamic arcuate nucleus of rats and mice within the first week of HFD feeding. Although these responses temporarily subsided, suggesting that neuroprotective mechanisms may initially limit the damage, with continued HFD feeding, inflammation and gliosis returned permanently to the mediobasal hypothalamus. Consistent with these data in rodents, we found evidence of increased gliosis in the mediobasal hypothalamus of obese humans, as assessed by MRI. These findings collectively suggest that, in both humans and rodent models, obesity is associated with neuronal injury in a brain area crucial for body weight control.
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