Characterization of the inflammatory and metabolic profile of adipose tissue in a mouse model of chronic hypoxia.

Rationale: In both obesity and chronic obstructive pulmonary disease altered oxygen tension in the adipose tissue (AT) has been suggested to dysfunction, subsequently contributing to metabolic complications. effects of chronic hypoxia on AT function will add to our understanding complex pathophysiology of alterations in AT inflammation, metabolism seen in both obesity and COPD. This study investigated the inflammatory metabolic profile of AT after chronic hypoxia. Methods: Fifty-two-week- C57Bl/6J mice were exposed to chronic hypoxia (8% O2) or normoxia for 21 after which AT and plasma were collected. Adipocyte size, AT gene inflammatory and metabolic genes, AT macrophage density and circulating concentrations were measured. Results: Food intake and body weight initiation of hypoxia. However, whereas food intake normalized after 10 lower body weight persisted. Chronic hypoxia markedly reduced AT mass adipocyte size. AT macrophage density and expression of Emr1, Ccl2, Lep was decreased, whereas Serpine1 and Adipoq expression levels were chronic hypoxia. Concomitantly, chronic hypoxia increased AT expression regulators of oxidative metabolism and markers of mitochondrial function lipolysis. Circulating IL-6 and PAI-1 concentrations were increased and concentration was decreased after chronic hypoxia. Conclusion: Chronic associated with decreased rather than increased AT inflammation, and decreased fat mass and adipocyte size. Furthermore, our data indicate chronic hypoxia is accompanied by significant alterations in AT expression, pointing towards an enhanced AT metabolic rate

Acute hydrogen sulfide–induced neuropathology and neurological sequelae: challenges for translational neuroprotective research

Hydrogen sulfide (H(2)S), the gas with the odor of rotten eggs, was formally discovered in 1777, over 239 years ago. For many years, it was considered an environmental pollutant and a health concern only in occupational settings. Recently, however, it was discovered that H(2)S is produced endogenously and plays critical physiological roles as a gasotransmitter. Although at low physiological concentrations it is physiologically beneficial, exposure to high concentrations of H(2)S is known to cause brain damage, leading to neurodegeneration and long‐term neurological sequelae or death. Neurological sequelae include motor, behavioral, and cognitive deficits, which are incapacitating. Currently, there are concerns about accidental or malicious acute mass civilian exposure to H(2)S. There is a major unmet need for an ideal neuroprotective treatment, for use in the field, in the event of mass civilian exposure to high H(2)S concentrations. This review focuses on the neuropathology of high acute H(2)S exposure, knowledge gaps, and the challenges associated with development of effective neuroprotective therapy to counteract H(2)S‐induced neurodegeneration