Vertical sleeve gastrectomy improves liver and hypothalamic functions in obese mice.

Vertical sleeve gastrectomy (VSG) is an effective surgery to treat obesity and diabetes. However, the direct effect of VSG on metabolic functions is not fully understood. We aimed to investigate if alterations in hypothalamic neurons were linked with perturbations in liver metabolism after VSG in an energy intake-controlled obese mouse model. C57BL/6 and hrNPY-GFP reporter mice received HFD for 12 weeks and were then divided into three groups: Sham (ad lib), sham (pair-fed) with VSG, and VSG. Food intake was measured daily, and blood glucose levels were measured before and after the study. Energy expenditure and body composition were determined. Serum parameters, liver lipid and glycogen contents were measured, and gene/protein expression were analyzed. Hypothalamic POMC, AgRP/NPY, and tyrosine hydroxylase expressing neurons were counted. As results, we found that VSG reduced body weight gain and adiposity induced by HFD, increased energy expenditure independent of energy intake. Fed and fasted blood glucose levels were reduced in the VSG group. While serum active GLP-1 level was increased, the active ghrelin and triglycerides levels were decreased along with improved insulin resistance in VSG group. Liver lipid accumulation, glycogen content, and gluconeogenic gene expression were reduced in the VSG group. In the hypothalamus, TH expressing neuron population was decreased, and the POMC-expressing neuron population was increased in the VSG group. Our data suggests that VSG improves metabolic symptoms by increasing energy expenditure and lowering lipid and glycogen contents in the liver. These physiological alterations are possibly related to changes in hypothalamic neuron populations.

Exercise induced Right Ventricular Fibrosis is Associated with Myocardial Damage and Inflammation.

BACKGROUND AND OBJECTIVES: Intense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF. METHODS: Sprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin (IL)-1ß and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles. RESULTS: After IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of pro-inflammation factors including IL-1ß and MCP-1 in the RV. CONCLUSIONS: Right ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.