Experimental and Clinical Endocrinology & Diabetes 

About: Experimental and Clinical Endocrinology & Diabetes is an academic journal published by Thieme Medical Publishers (Germany). The journal publishes majorly in the area(s): Diabetes mellitus & Insulin. It has an ISSN identifier of 0947-7349. Over the lifetime, 4381 publications have been published receiving 74876 citations. The journal is also known as: Experimental and clinical endocrinology and diabetes (Internet) & Experimental and clinical endocrinology and diabetes.

Role of brain insulin receptor and control of body weight and reproduction

Abstract: Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.

Adipose tissue dysfunction in obesity.

Abstract: The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.

Energy on demand

Abstract: Goals Reduce greenhouse gas emissions to 1990 levels by 2020. All new residential buildings meet zero-­‐net-­‐energy (ZNE) goals by 2020, all new commercial buildings by 2030. Why it is Important Combustion of fossil fuels to power vehicles and buildings is the largest source of greenhouse gas emissions in the state. Energy use in residential and commercial buildings and the industrial sector is the second largest source of greenhouse gas (GHG) emissions in California. California has significantly reduced building energy demand through a series of progressive appliance and building standards that promote energy efficiency. These standards, combined with the state's mild climate, mean that California has among the lowest per capita electricity consumption rates of any state in the nation. In 2011, California had the fifth lowest per capita energy demand of any state. 1 Recent Trends Energy consumption occurs in all sectors of state's economy. In California, the transportation sector accounts for the highest share of the state's energy consumption. This demand is met, primarily, through the combustion of fossil fuels to power passenger cars and trucks. Consumption in the industrial, commercial, and industrial sectors is primarily accounted for by electricity and natural gas consumption. 1 Electricity use per capita in California is well below the national average 2 , owing to the state's appliance and building energy efficiency standards and mild climate. Even as the state's population has continued to grow, per capita electricity use has remained steady, while the national average has increased slightly. When comparing per capita energy consumption by sector, it is clear that California's energy efficiency efforts have been most successful in the building sector.

Definition, Classification and Diagnosis of Diabetes Mellitus

Abstract: Aim of recommendations like this one issued by the German Diabetes Association is to provide the GP and diabetologist and his team with information he needs for his daily practice. These recommendations are updated annually. They are written by a group of experts, but they are not evidence based guidelines. This specific recommendation for diabetes diagnosis briefly describes the diabetes types and the different options for diagnosis. Also the caveats and the practical procedure are presented.

Mechanisms of TNF-alpha-induced insulin resistance.

Abstract: There is now substantial evidence linking TNF-alpha to the presentation of insulin resistance in humans, animals and in vitro systems. We explored the relationship between TNF-alpha and insulin resistance using knockout mice deficient for either TNF-alpha or one or both of its receptors, p55 and p75. In studies of TNF-alpha-deficient knockout mice with diet-induced obesity, obese TNF-alpha knockouts responded to an exogenous dose of insulin or glucose much more efficiently than TNF-alpha wild-type animals. This finding suggests that deletion of TNF-alpha leads to increased insulin sensitivity, ie decreased insulin resistance. In studies using genetically obese ob/ob mice, TNF-alpha receptor wild-type and p75 receptor knockout animals developed a pronounced hyperinsulinemia and transient hyperglycaemia, whereas p55 receptor and double-knockout animals did not. Moreover, in glucose and insulin tolerance tests, we found that p75 knockout animals exhibited profiles identical to those of the wild-type animals, but that p55 knockout animals and double mutants showed a mild improvement in insulin sensitivity, relative to the wild type. Since the improvement in sensitivity was slightly greater with double mutants, p55 alone cannot be responsible for TNF-alpha's promotion of insulin resistance in obese mice, despite the likelihood that it is more important than p75. How TNF-alpha-related insulin resistance is mediated is not fully clear, although phosphorylation of serine residues on IRS-1 has previously been shown to be important. When we monitored Glut 4 expression in obese TNF-alpha wild-type and knockout mice, we found no convincing evidence that TNF-alpha mediation of the down-regulation of Glut 4 mRNA expression is responsible for insulin resistance. However, we found an approximately 2-fold increase in insulin-stimulated tyrosine phosphorylation of the insulin receptor in the muscle and adipose tissue of TNF-alpha knockout mice, suggesting that insulin receptor signalling is an important target for TNF-alpha. Other possible mediators of TNF-alpha-induced insulin resistance include circulating free fatty acids (FFAs) and leptin.