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This was further confirmed by increased weight of both white and brown adipose tissues in female BACHD mice compared to WT mice (see Table S1 available online). Obesity can be the result of reduced activity, increased food intake, a reduced metabolic rate, or a combination of these factors. BACHD mice did not display reduced general activity Enol in the open field at 4?months of age, a time point when they were already significantly obese (total line crossings/30 min, 2660?�� 150 in BACHD versus 2550?�� 120 in WT mice; n?= 8/genotype; n.s.). However, already at 2?months of age, both male and female BACHD mice displayed a significantly higher food intake as compared to WT mice, and this difference persisted at 4?months of age (Figure?1C). When the metabolic rate was assessed using indirect calorimetry, female BACHD mice were found to have similar oxygen consumption as WT littermates; however, the respiratory quote was lower, indicating an obesity-induced compensatory increase in lipid oxidation (Figure?1D). Taken together, these data showed that BACHD mice developed obesity as a result of chronically increased food intake. Next, we sought to determine which endocrine abnormalities accompanied the obese phenotype. Female BACHD mice displayed significantly buy SNS-032 increased basal glucose levels (10.03?�� 0.21?mmol/l; n?= 6) compared to WT mice (9.05?�� 0.35; n?= 6) (p?http://www.selleckchem.com/screening/fda-approved-drug-library.html that serum levels of leptin were severely elevated in BACHD mice, indicative of leptin resistance (Table S2). Reduced leptin sensitivity in the CNS of BACHD was confirmed by reduced p-Stat3 activation in the hypothalamus after an i.p. injection of leptin in BACHD mice compared to WT mice (Figure?S1). Other peripheral factors related to appetite control and adipose tissue metabolism such as interleukin 6 (IL-6) and ghrelin, as well as nonesterified free fatty acids (NEFAs) or triglycerides, were not altered in serum (Table S2). Cholesterol and adiponectin levels were increased in female BACHD mice (Table S2). To test the hypothesis that hypothalamic expression of mutant htt was responsible for the development of metabolic disturbances in BACHD mice, we used recombinant adeno-associated viral vectors of serotype 5 (rAAV5) to selectively express a large N-terminal fragment of the mutant htt protein in the hypothalamic region of adult mice of the FVB/N strain.