Background/objectives: Hypothalamic neurons play a major role in the control of body mass. Obese subjects present radiologic signs of gliosis in the hypothalamus, which may reflect the damage or loss of neurons involved in whole-body energy homeostasis. It is currently unknown if hypothalamic gliosis (1) differs between obese nondiabetic (ND) and obese diabetic subjects (T2D) or (2) is modified by extensive body mass reduction via Roux-n-Y gastric bypass (RYGB).
Subjects/methods: Fifty-five subjects (all female) including lean controls (CT; n = 13), ND (n = 28), and T2D (n = 14) completed at least one study visit. Subjects underwent anthropometrics and a multi-echo MRI sequence to measure mean bilateral T2 relaxation time in the mediobasal hypothalamus (MBH) and two reference regions (amygdala and putamen). The obese groups underwent RYGB and were re-evaluated 9 months later. Analyses were by linear mixed models.
Results: Analyses of T2 relaxation time at baseline showed a group by region interaction only in the MBH (P < 0.0001). T2D had longer T2 relaxation times compared to either CT or ND groups. To examine the effects of RYGB on hypothalamic gliosis a three-way (group by region by time) mixed effects model adjusted for age was executed. Group by region (P < 0.0001) and region by time (P = 0.0005) interactions were significant. There was a reduction in MBH relaxation time by RYGB, and, although the T2D group still had higher T2 relaxation time overall compared to the ND group, the T2D group had significantly lower T2 relaxation time after surgery and the ND group showed a trend. The degree of reduction in MBH T2 relaxation time by RYGB was unrelated to clinical outcomes.
Conclusion: T2 relaxation times, a marker of hypothalamic gliosis, are higher in obese women with T2D and are reduced by RYGB-induced weight loss.
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http://dx.doi.org/10.1038/s41366-019-0399-8 | DOI Listing |
Curr Obes Rep
January 2025
Department of Medicine, University of Washington, Seattle, WA, USA.
Purpose Of Review: To evaluate the role of hypothalamic inflammation and gliosis in human obesity pathogenesis and other disease processes influenced by obesity.
Recent Findings: Recent studies using established and novel magnetic resonance imaging (MRI) techniques to assess alterations in hypothalamic microarchitecture in humans support the presence of hypothalamic inflammation and gliosis in adults and children with obesity. Studies also identify prenatal exposure to maternal obesity or diabetes as a risk factor for hypothalamic inflammation and gliosis and increased obesity risk in offspring.
J Neurochem
January 2025
Department of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
medRxiv
September 2024
Department of Medicine, University of Washington, Seattle, WA.
Background: Hypothalamic gliosis is mechanistically linked to obesity and insulin resistance in rodent models. We tested cross-sectional associations between radiologic measures of hypothalamic gliosis in humans and clinically relevant cardiovascular disease risk factors, as well as prevalent coronary heart disease.
Methods: Using brain MRI images from Framingham Heart Study participants (N=867; mean age, 55 years; 55% females), T2 signal intensities were extracted bilaterally from the region of interest in the mediobasal hypothalamus (MBH) and reference regions in the amygdala (AMY) and putamen (PUT).
Neoplasia
November 2024
Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital of Southern Medical University, Guangzhou, China. Electronic address:
Diabetes
December 2024
Department of Biological Sciences, Wayne State University, Detroit, MI.
The prevalence of type 2 diabetes (T2D) poses a significant health challenge, yet the contribution of air pollutants to T2D epidemics remains under-studied. Several studies demonstrated a correlation between exposure to volatile organic compounds (VOCs) in indoor/outdoor environments and T2D. Here, we conducted the first meta-analysis, establishing a robust association between exposure to benzene, a prevalent airborne VOC, and insulin resistance in humans across all ages.
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