High altitude (HA) presents inhospitable environmental conditions that adversely affects human physiology and metabolism. Changes in physiological functions are reported during high altitude exposure, but the changes vary with physical state, culture habits, geographical locations, and genetic variation of individual. The present study was carried out to explore the variation in acclimatization pattern of two different ethnic groups in relation to cardiovascular functions, lipid profile and body composition. The study was carried out on 30 human volunteers (20 Indian and 10 Kyrgyz) initially at Bishkek for basal recording and on day 3, 7, 14, and 21 of high altitude (3200 m) induction and again on day 3 of de-induction. On altitude exposure significant decrease in body weight was observed both in Indian (day 14, p<0.001) and Kyrgyz (day 3, p<0.01) subjects. Decreased levels of total body water, extra cellular and intra cellular body water were also observed in both the groups. Significant reduction in body mass index (p<0.01), fat free mass (p<0.01), body cell mass (p<0.01) and body volume (p<0.01) was also observed in Kyrgyz subjects, whereas in Indian subjects the changes were not significant in these variables on high altitude exposure. Diastolic blood pressure and heart rate increased significantly on day 3 (p<0.001 and p<0.01, respectively) of induction in Indian subjects; whereas in Kyrgyz significant increase was observed on day 14 (p<0.05) in both the cases. High density lipoprotein (HDL) cholesterol levels increased significantly on day 7 of HA exposure in both the groups. Results indicate that the Indian and Kyrgyz groups report differently, in relation to changes in cardiovascular functions, lipid profiles, and body composition, when exposed to HA. The difference observed in acclimatization pattern in the two groups may be due to ethnic/genetic variation of two populations.

Bone morphogenetic protein 7 (BMP7), also known as osteogenic protein-1 (OP-1) is a member of Transforming growth factor-β (TGF-β) family of proteins. Bone morphogenetic proteins were discovered in 1965 by Marshal Urist, of which BMP7 is of particular interest in this review being a leptin-independent anorexinogen and having role in energy expenditure in the brown adipose tissue, which makes it a potential target for preventing/treating obesity. As it has been established that Obesity displays a state of leptin-resistance, thus a protein-like BMP7 which acts through a leptin-independent pathway could give new therapeutic directions. This review will also discuss the synthesis and action of BMP7, along with its receptors and signal transduction. A brief note about BMP7-mediated brown fat development and energy balance is also discussed.

PRMT1 might have a potential importance as a therapeutic target for the treatment of HH-induced maladies.

Background and aims There is significant overlap between non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD) with regards to risk factors and disease progression. However, the mechanism by which fatty liver disease arises from concomitant obesity and overconsumption of alcohol (syndrome of metabolic and alcohol-associated fatty liver disease; SMAFLD), is not fully understood. Methods Male C57BL6/J mice were fed chow diet (Chow) or high-fructose, high-fat, high-cholesterol diet (FFC) for 4 weeks, then administered either saline or ethanol (EtOH, 5% in drinking water) for another 12 weeks. The EtOH treatment also consisted of a weekly 2.5 g EtOH/kg body weight gavage. Markers for lipid regulation, oxidative stress, inflammation, and fibrosis were measured by RT-qPCR, RNA-seq, Western blot, and metabolomics. Results Combined FFC-EtOH induced more body weight gain, glucose intolerance, steatosis, and hepatomegaly compared to Chow, EtOH, or FFC. Glucose intolerance by FFC-EtOH was associated with decreased hepatic protein kinase B (AKT) protein expression and increased gluconeogenic gene expression. FFC-EtOH increased hepatic triglyceride and ceramide levels, plasma leptin levels, hepatic Perilipin 2 protein expression, and decreased lipolytic gene expression. FFC and FFC-EtOH also increased AMP-activated protein kinase (AMPK) activation. Finally, FFC-EtOH enriched the hepatic transcriptome for genes involved in immune response and lipid metabolism. Conclusions In our model of early SMAFLD, we observed that the combination of an obesogenic diet and alcohol caused more weight gain, promoted glucose intolerance, and contributed to steatosis by dysregulating leptin/AMPK signaling. Our model demonstrates that the combination of an obesogenic diet with a chronic-binge pattern alcohol intake is worse than either insult alone.

No abstract