Sexuality Minority Status, Victimization, Mental Health, and Substance Use.

Prior research suggests that sexual minority status is related to victimization, mental health issues, and substance use. However, few studies have sought to connect these relationships in a way supported by theory, and fewer have utilized probability and/or nationally representative samples. The current study seeks to test the relationships among these variables, guided by general strain theory (GST).

SIRT3 overexpression in rat muscle does not ameliorate peripheral insulin resistance.

Reduced expression of the NAD+-dependent deacetylase, SIRT3, has been associated with insulin resistance and metabolic dysfunction in humans and rodents. In this study, we investigated whether specific overexpression of SIRT3 in vivo in skeletal muscle could prevent high-fat diet (HFD)-induced muscle insulin resistance. To address this, we used a muscle-specific adeno-associated virus (AAV) to overexpress SIRT3 in rat tibialis and extensor digitorum longus (EDL) muscles.

Case Study of a Comprehensive Team-Based Approach to Increase Colorectal Cancer Screening.

Introduction: Colorectal cancer is the second leading cause of cancer deaths among men and women in West Virginia. In addition, 51% of all colorectal cancers diagnosed in West Virginia from 2012 to 2016 were detected at either regional (31%) or distant (20%) stages indicating a need for improved early detection.

Methods: West Virginia University Cheat Lake Physicians participated in the West Virginia Program to Increase Colorectal Cancer Screening, a program of Cancer Prevention and Control at the WVU Cancer Institute.

Liver-specific overexpression of SIRT3 enhances oxidative metabolism, but does not impact metabolic defects induced by high fat feeding in mice.

The mitochondrial enzyme SIRT3 is an NAD-dependent deacetylase important in cell metabolism, and a decline in its protein expression or activity has been linked with insulin resistance in obesity, ageing and type 2 diabetes. While studies in SIRT3 knockout mice have dramatically improved our understanding of the function of SIRT3, the impact of increasing SIRT3 levels remains under-examined. In this study we investigated the effects of liver-specific SIRT3 overexpression in mice on mitochondrial function and metabolic profile in both isolated hepatocytes and in vivo.

Leveraging Electronic Health Records Data for Enhanced Colorectal Cancer Screening Efforts.

Introduction: Colorectal cancer is the third most common type of cancer in the United States for men and women combined. While the current threat of disease nationally is significant, the majority of colorectal cancer cases and deaths could be prevented through established screening tests and guidelines. Within the Appalachian region and West Virginia in particular, colorectal cancer is a significant public health problem.

Transcriptional programming of lipid and amino acid metabolism by the skeletal muscle circadian clock.

Circadian clocks are fundamental physiological regulators of energy homeostasis, but direct transcriptional targets of the muscle clock machinery are unknown. To understand how the muscle clock directs rhythmic metabolism, we determined genome-wide binding of the master clock regulators brain and muscle ARNT-like protein 1 (BMAL1) and REV-ERBα in murine muscles. Integrating occupancy with 24-hr gene expression and metabolomics after muscle-specific loss of BMAL1 and REV-ERBα, here we unravel novel molecular mechanisms connecting muscle clock function to daily cycles of lipid and protein metabolism.

Increased mitochondrial calcium uniporter in adipocytes underlies mitochondrial alterations associated with insulin resistance.

Intracellular calcium influences an array of pathways and affects cellular processes. With the rapidly progressing research investigating the molecular identity and the physiological roles of the mitochondrial calcium uniporter (MCU) complex, we now have the tools to understand the functions of mitochondrial Ca in the regulation of pathophysiological processes. Herein, we describe the role of key MCU complex components in insulin resistance in mouse and human adipose tissue.

Overexpression of SIRT1 in rat skeletal muscle does not alter glucose induced insulin resistance.

SIRT1 is a NAD+-dependent deacetylase thought to regulate cellular metabolic pathways in response to alterations in nutrient flux. In the current study we investigated whether acute changes in SIRT1 expression affect markers of muscle mitochondrial content and also determined whether SIRT1 influenced muscle insulin resistance induced by acute glucose oversupply. In male Wistar rats either SIRT1 or a deacetylase inactive mutant form (H363Y) was electroprated into the tibialis cranialis (TC) muscle.

Erratum to "Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock" [Mol Metab 3 (2014) 29-41].

[This corrects the article DOI: 10.1016/j.molmet.

Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock.

Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation.

The evolution of insulin resistance in muscle of the glucose infused rat.

Glucose infusion into rats causes skeletal muscle insulin resistance that initially occurs without changes in insulin signaling. The aim of the current study was to prolong glucose infusion and evaluate other events associated with the transition to muscle insulin resistance. Hyperglycemia was produced in rats by glucose infusion for 3, 5 and 8 h.

Enhancement of muscle mitochondrial oxidative capacity and alterations in insulin action are lipid species dependent: potent tissue-specific effects of medium-chain fatty acids.

Objective: Medium-chain fatty acids (MCFAs) have been reported to be less obesogenic than long-chain fatty acids (LCFAs); however, relatively little is known regarding their effect on insulin action. Here, we examined the tissue-specific effects of MCFAs on lipid metabolism and insulin action.

Research Design And Methods: C57BL6/J mice and Wistar rats were fed either a low-fat control diet or high-fat diets rich in MCFAs or LCFAs for 4-5 weeks, and markers of mitochondrial oxidative capacity, lipid levels, and insulin action were measured.