OBJECTIVE Racial differences in BMI increase with education. Weight perception may be an important factor in overweight and obesity in black women. The aim of this study was to determine the mediating role of weight underassessment on race differences in BMI in college graduates compared with non-college graduates. METHODS Weight perception was assessed among respondents to the 2007-2014 National Health and Nutrition Examination Survey (n = 4,871). Those who had BMI-assessed overweight or obesity and self-assessed underweight or about-right weight underassessed their weight. The associations between race and BMI through weight underassessment by college graduate status were determined using a moderated mediation analysis. RESULTS Black women had higher BMI than white women (β = 2.72, SE = 0.28), and disparities were larger in college graduates (β = 3.50, SE = 0.25) compared with non-college graduates (β = 0.78, SE = 0.15). Non-college graduate black women were more likely to underassess their weight (z score = 0.43, SE = 0.05). Indirect associations between race and BMI through weight underassessment were found only among non-college graduates (z score = -0.02, SE = 0.01), but race differences in BMI remained after accounting for weight perception among college graduates and non-college graduates. CONCLUSIONS This study demonstrates that a nuanced, intersectional understanding of weight perception and BMI among women is required to address racial disparities in obesity. © 2020 The Obesity Society.Obeticholic acid (OCA) activates the farnesoid X receptor (FXR) to lower circulating total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) concentrations and to stimulate fecal cholesterol excretion in mice by increasing hepatic SR-B1 expression. Here we show that hepatic SR-B1 depletion by an adenovirus expressing Sr-b1 shRNA (Ad-shSR-B1) attenuated these beneficial effects of OCA in mice on a chow diet.  https://www.selleckchem.com/products/epoxomicin-bu-4061t.html  The mRNA levels of ABC cholesterol transporter genes (Abca1, Abcg1, Abcg5, and Abcg8) were unchanged in the liver of hepatic SR-B1-depleted mice regardless of OCA treatment; however, a modest increase in Abca1, Abcg5, and Abcg8 mRNA levels was observed in the ileum of vehicle-treated control mice and Abca1 and Abcg8 mRNA levels were increased more by OCA administration. OCA treatment of Sr-b1 knock out (KO) mice (Sr-b1-/-) fed a normal chow diet (NCD) displayed a similar lack of transhepatic cholesterol movement, as well as a modest increase in the levels of ileum cholesterol transporter expression. However, OCA treatment of Sr-b1 KO mice fed a cholesterol-enriched diet reduced circulating cholesterol and increased fecal cholesterol output to comparable degrees to that of wild-type (WT) mice, and these effects were accompanied by substantial elevations of mRNA levels of Abca1, Abcg1, Abcg5, and Abcg8 in the ileum of Sr-b1 KO mice. Our studies suggest that FXR activation stimulates intestinal cholesterol excretion and reduces diet-induced hyperlipidemia through increased expression of ileal cholesterol transporters when hepatic SR-B1-mediated cholesterol movement is absent. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.Cancer cachexia is the loss of lean muscle mass with or without loss of fat mass that is often highlighted by a progressive loss of skeletal muscle mass and function. The mechanisms behind the cachexia-related loss of skeletal muscle are poorly understood, including cachexia-related muscle functional impairments. Existing models have revealed some potential mechanisms, but appear limited to how the cancer develops and the type of tumors that form. We studied the C57BL6/J (B6) ApcMin/+ TgFabp1-Cre TGPIK3ca* (CANCER) mouse. In this model, mice develop highly aggressive intestinal cancers. We tested whether CANCER mice develop cancer cachexia, if muscle function is altered and if sex differences are present. Both female and male mice, B6 (CONTROL) and CANCER mice, were analyzed to determine body weight, hindlimb muscle mass, protein concentration, specific force, and fatigability. Female CANCER mice had reduced body weight and hindlimb muscle mass compared with female CONTROL mice, but lacked changes in protein concentration and specific force. Male CANCER mice had reduced protein concentration and reduced specific force, but lacked altered body weight and muscle mass. There were no changes in fatigability in either group. Our study demonstrates that CANCER mice present an early stage of cachexia, have reduced specific force in male CANCER mice and develop a sex-dependent cachexia phenotype. However, CANCER mice lack certain aspects of the syndrome seen in the human scenario and, therefore, using the CANCER mice as a preclinical model does not seem sufficient in order to maximize the translation of preclinical findings to humans. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.BACKGROUND Severe peripheral angiopathy in diabetic patients is a major contributing factor for low response rate to phosphodiesterase-5 inhibitors. OBJECTIVES To examine whether and how Dickkopf3 (DKK3), a secreted modulator of the Wnt pathway that known to be involved in endothelial cell repair and vascular progenitor cell migration, restores erectile function in diabetic mice. METHODS Eight-week-old C57BL/6 mice were received intraperitoneal injections of streptozotocin (50 mg/kg for 5 days). Eight weeks after the diabetes was induced, the efficacy of DKK3 determined by three independent experiments experiment 1 (DKK3 peptide [5 μg in 20 μL PBS); experiment 2 (DKK3 plasmid DNA with electroporation [10 μg, 40 μg, or 100 μg in 20 μL PBS, respectively]; and experiment 3 (DKK3 adenovirus [1 × 107 , 1 × 108 , 1 × 109 virus particles per 20 μL, respectively]). Erectile function was measured by electrical stimulation of the cavernous nerve one week (for peptide) or two weeks (for genes) after treatment. The angiogenic activity of DKK3 was determined in diabetic penis in vivo and in primary cultured mouse cavernous endothelial cells (MCECs) in vitro.