![Lzip pgc1a](https://loka.nahovitsyn.com/70.jpg)
Racette S.B., Weiss E.P., Schechtman K.B., Steger-May K., Villareal D.T., Obert K.A., Holloszy J.O. Trends in Obesity Prevalence by Race and Hispanic Origin-1999–2000 to 2017–2018. Ogden C.L., Fryar C.D., Martin C.B., Freedman D.S., Carroll M.D., Gu Q., Hales C.M. Genotype x Surgery p < 0.05 interaction of genotype and surgery, & p < 0.05 main effect of HBV, & p < 0.05 sham vs. Individual data points and the group means ± SEM are displayed ( n = 7–12). Based on the change in fat- and fat-free mass the ( F) metabolic efficiency of weight gain was calculated as the sum of the energy content of fat and fat-free mass multiplied by the respective changes over the one-week HFHS diet, divided by the one-week energy intake. A quantitative MRI was utilized to determine fat- and fat-free mass at the initiation and end of the one-week HFHS diet, and the change in fat mass ( D) and the fat-free mass ( E) are presented. ( C) Energy intake was calculated as the energy density of the HFHS diet multiplied by the one-week food intake. ( B) Feed efficiency was determined as the body weight gained divided by the energy intake during the one-week HFHS diet. Male WT and LPGC1a mice underwent sham or HBV surgery, and were administered a one-week HFHS diet following recovery. These data demonstrate a sex-specific role of reduced liver energy metabolism in acute diet-induced weight gain, and the need for a more nuanced assessment of the role of vagal signaling in short-term diet-induced weight gain.Įnergy expenditure energy homeostasis food intake liver mitochondria weight gain.ĭisruption of liver vagal innervation by common hepatic branch vagotomy increases short-term diet-induced weight gain in WT, but not LPGC1a, male mice. HBV increased HFHS-induced weight gain (85%, p < 0.05) in male WT mice, but not LPGC1a mice. WT and LPGC1a mice underwent sham surgery or HBV to assess whether vagal signaling was involved in the HFHS-induced weight gain of male LPGC1a mice. The greater weight gain was associated with altered feeding behavior and lower activity energy expenditure during the HFHS diet in LPGC1a males. LPGC1a male, but not female, mice had a 70% greater high-fat/high-sucrose (HFHS) diet-induced weight gain compared to wildtype (WT) mice ( p < 0.05).
![lzip pgc1a lzip pgc1a](https://images.novusbio.com/fullsize2/PGC1-alpha-Antibody-Flow-Cytometry-NBP1-04676-img0021.jpg)
Herein, we used a hepatocyte PGC1a heterozygous (LPGC1a) mouse model, with associated reductions in mitochondrial fatty acid oxidation and respiratory capacity, to assess the role of liver energy metabolism in systemic energy homeostasis. However, possible offsite actions of the chemical compounds confound the precise role of liver energy metabolism. Previously, increased acute food intake following the chemical reduction of hepatic fatty acid oxidation and ATP levels was prevented by common hepatic branch vagotomy (HBV). The central integration of peripheral neural signals is one mechanism by which systemic energy homeostasis is regulated.
![Lzip pgc1a](https://loka.nahovitsyn.com/70.jpg)