Oncostatin M modulation of lipid storage

© 2015 by the authors; licensee MDPI, Basel, Switzerland. Oncostatin M (OSM) is a cytokine belonging to the gp130 family, whose members serve pleiotropic functions. However, several actions of OSM are unique from those of other gp130 cytokines, and these actions may have critical roles in inflammatory mechanisms influencing several metabolic and biological functions of insulin-sensitive tissues. In this review, the actions of OSM in adipose tissue and liver are discussed, with an emphasis on lipid metabolism

Relationships Between Interprofessional Teamwork and Clinical Management of

Diabetes mellitus (DM) is a highly prevalent chronic disease that affects 29 million people in the United States including over 2 million veterans who receive care through the Veterans Administration. Patient-aligned care teams (PACTs) are an interprofessional teamwork system designed to improve outcomes of chronic illness, but empirical explorations of the efficacy of the PACTs have been insufficient. Utilizing the chronic care model, the purpose of this retrospective study was to determine if PACTs have been efficient in the diabetic management of veterans receiving care through a Southeastern VA. Medical records for 114 veterans with type 2 DM were randomly selected. A 1-way ANOVA was used to analyze outcomes for 5 evidence-based standards (SBP, DBP, BGL, A1C, & LDL) among 6 outpatient clinics. A repeated measures ANOVA was used for the same 5 evidence-based standards for the clinics to assess if there were any changes from FY2014 to FY2016. Results revealed that blood pressure readings and LDL levels met evidence-based standards, while A1C and BGL levels did not. No significant differences over the 3-year period were noted nor were there significant differences in patterns of performance between the clinics. The findings provide an essential basis for initiating a discussion on the potential of PACTs for the delivery of quality healthcare to U.S. veterans with diabetes and other chronic diseases. Positive social change can result from improving the delivery of healthcare using the PACT model to decrease morbidity, improve clinical outcomes, and increase the quality of life of U.S. veterans with type 2 DM. Future research that examines perceptions of clinical team members, team stability, and the delivery of shared care is warranted

The Fat Controller: Adipocyte Development

Obesity is a condition characterized by excess adipose tissue that results from positive energy balance and is the most common metabolic disorder in the industrialized world. The obesity epidemic shows no sign of slowing, and it is increasingly a global problem. Serious clinical problems associated with obesity include an increased risk for type 2 diabetes, atherosclerosis, and cancer. Hence, understanding the origin and development of adipocytes and adipose tissue will be critical to the analysis and treatment of metabolic diseases. Historically, albeit incorrectly, adipocytes were thought to be inert cells whose singular function was lipid storage. It is now known that adipocytes have other critical functions; the most important include sensitivity to insulin and the ability to produce and secrete adipocyte-specific endocrine hormones that regulate energy homeostasis in other tissues. Today, adipocytes are recognized as critical regulators of whole-body metabolism and known to be involved in the pathogenesis of a variety of metabolic diseases. All cells come from other cells and many cells arise from precursor cells. Adipocytes are not created from other adipocytes, but they arise from precursor cells. In the last two decades, scientists have discovered the function of many proteins that influence the ability of precursor cells to become adipocytes. If the expansion of the adipose tissue is the problem, it seems logical that adipocyte development inhibitors could be a viable anti-obesity therapeutic. However, factors that block adipocyte development and limit adipocyte expansion also impair metabolic health. This notion may be counterintuitive, but several lines of evidence support the idea that blocking adipocyte development is unhealthy. For this reason it is clear that we need a better understanding of adipocyte development. © 2012 Jacqueline M

The Importance of Sexual Education on Adolescent Sexual Behaviors

Objective: The objective of this report is to examine how sex education for adolescents living in rural and urban settings in the states of Alabama and Ohio impacts their sexual health and behaviors. Methods: To explore this topic, several different statistical tests were done: an independent t-test, an ANOVA test, a Pearman/Spearman correlation, a regression, and a standard correlation. The reason for these different tests was to compare the difference in the number of sexually transmitted diseases, how insurance status correlates with teenage pregnancy rates and sexually transmitted diseases, and the relationship between socioeconomic status and the rate of sexually transmitted diseases. Results: We found that there are a multitude of factors that influence sexual behaviors and health of teenagers: the type of county they live in (rural or urban), their socioeconomic status, insurance status, and type of household. Therefore, it is imperative that these healthcare disparities are combated so that underserved teenage patient populations can have improved rates of sexual health and have access to sexual health resources that can enhance their health status and overall patient care outcomes

STAT1, NF-κB and ERKs play a role in the induction of lipocalin-2 expression in adipocytes

Lipocalin-2 (LCN2) is induced in conditions of obesity and Type 2 diabetes (T2DM). IFNγ and TNFα induce LCN2 expression in adipocytes in a manner that is dependent on transcription. The effects of these cytokines are additive. IFNγ induced STAT1 and TNFα induced NF-κB play a role in the induction of LCN2. In the LCN2 promoter, one NF-κB binding site and four STAT1 binding sites were identified by in silico and in vitro approaches. MAPK (ERKs 1 and 2) activation was required for the IFNγ and TNFα induction of LCN2 expression, but did not affect the nuclear translocation or DNA binding activity of STAT1 or NF-κB. The NF-κB binding site and the STAT1 binding sites we identified in vitro were confirmed by in vivo studies. Transfection of a LCN2 promoter/luciferase reporter construct confirmed acute activation by IFNγ and TNFα. Our studies identify mechanisms involved in the actions of cytokines secreted from immune cells in adipose tissue that induce LCN2 expression in conditions of obesity and T2DM. © 2013 Elsevier GmbH

Induction of SOCS-3 is insufficient to confer IRS-1 protein degradation in 3T3-L1 adipocytes

Insulin receptor substrate (IRS)-1 is a key protein in insulin signaling. Several studies have shown that the expression of IRS-1 can be modulated by protein degradation via the proteasome and the degradation of IRS-1 can be related to insulin-resistant states. The degradation of IRS-1 has been shown to be induced by SOCS-1 and SOCS-3 via the ubiquitin pathway. The goal of our study was to determine if the induction of SOCS-3 correlated with increased IRS-1 degradation in cultured 3T3-L1 adipocytes. Interestingly, our studies have shown that there is little correlation between the induction in SOCS-3 expression and the degradation of IRS-1 in mature 3T3-L1 adipocytes. Our results clearly demonstrate that treatment with leukemia inhibitory factor (LIF) or cardiotrophin (CT)-1 strongly induces the expression of SOCS-3 in mature 3T3-L1 adipocytes, but does not affect the degradation of IRS-1. On the contrary, tumor necrosis factor (TNF) α and insulin, which very weakly induce SOCS-3 expression, have profound effects on IRS-1 degradation. In summary, our results indicate that the expression of SOCS-3 does not correlate with the degradation of IRS-1 proteins in fat cells. © 2006 Elsevier Inc. All rights reserved

Diosgenin, 4-hydroxyisoleucine, and fiber from fenugreek: Mechanisms of actions and potential effects on metabolic syndrome

© 2015 American Society for Nutrition. Metabolic syndrome and its complications continue to rise in prevalence and show no signs of abating in the immediate future. Therefore, the search for effective treatments is a high priority in biomedical research. Products derived from botanicals have a time-honored history of use in the treatment of metabolic diseases including type 2 diabetes. Trigonella foenum-graecum, commonly known as fenugreek, is an annual herbaceous plant that has been a staple of traditional herbal medicine in many cultures. Although fenugreek has been studied in both clinical and basic research settings, questions remain about its efficacy and biologic mechanisms of action. Diosgenin, 4-hydroxyisoleucine, and the fiber component of the plant are the most intensively studied bioactive constituents present in fenugreek. These compounds have been demonstrated to exert beneficial effects on several physiologic markers including glucose tolerance, inflammation, insulin action, liver function, blood lipids, and cardiovascular health. Although insights into the molecular mechanisms underlying the favorable effects of fenugreek have been gained, we still do not have definitive evidence establishing its role as a therapeutic agent in metabolic disease. This review aims to summarize the currently available evidence on the physiologic effects of the 3 best-characterized bioactive compounds of fenugreek, with particular emphasis on biologic mechanisms of action relevant in the context of metabolic syndrome

Adipogenesis

Adipose tissue is an important site for lipid storage, energy homeostasis, and whole-body insulin sensitivity. It is important to understand the mechanisms involved in adipose tissue development and function, which can be regulated by the endocrine actions of various peptide and steroid hormones. Recent studies have revealed that white and brown adipocytes can be derived from distinct precursor cells. This review will focus on transcriptional control of adipogenesis and its regulation by several endocrine hormones. The general functions and cellular origins of adipose tissue and how the modulation of adipocyte development pertains to metabolic disease states will also be considered. © 2012 Cold Spring Harbor Laboratory Press; all rights reserved

2-deoxyglucose inhibits induction of chemokine expression in 3T3-L1 adipocytes and adipose tissue explants

© 2016 The Obesity Society Objective: To determine the influence of glycolytic inhibition on the adipocyte inflammatory response. Methods: To determine the effect of 2-deoxyglucose (2-DOG) on the inflammatory response, mature 3T3-L1 adipocytes were co-treated with 2-DOG and LPS or TNF. To determine the effect of endoplasmic reticulum stress on TNF-induced induction of chemokines, adipocytes were pretreated with thapsigargin or salubrinal. Chemokine mRNA levels were determined using quantitative real-time PCR, and secretion of CCL2 was determined by Western blot. Results: 2-DOG treatment reduced the ability of LPS and TNF to induce CCL2 mRNA levels and reduced secreted CCL2 protein levels in a dose-dependent manner. A similar pattern of mRNA regulation was observed for other chemokines. The attenuation of TNF-induced CCL2 mRNA levels occurred regardless of whether glucose or pyruvate was present in the media, suggesting that mechanisms other than glycolysis might mediate the observed effects. Treatment with the endoplasmic reticulum stressor thapsigargin and the endoplasmic reticulum signaling activator salubrinal reduced chemokine mRNA levels similarly to 2-DOG. Conclusions: Collectively, our data indicate that 2-DOG suppresses inflammatory chemokine induction in adipocytes. The effects of 2-DOG do not seem to be linked to glycolysis but correlate with endoplasmic reticulum stress activation