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Obesity develops as a result of altered energy homeostasis favoring fat storage. Here we describe a new transcription co-regulator for adiposity and energy metabolism, SERTA domain containing 2 (TRIP-Br2, also called SERTAD2). TRIP-Br2-null mice are resistant to obesity and obesity-related insulin resistance. Adipocytes of these knockout mice showed greater stimulated lipolysis secondary to enhanced expression of hormone sensitive lipase (HSL) and b3-adrenergic (Adrb3) receptors. The knockout mice also have higher energy expenditure because of increased adipocyte thermogenesis and oxidative metabolism caused by upregulating key enzymes in their respective processes. Our data show that a cell-cycle transcriptional co-regulator, TRIP-Br2, modulates fat storage through simultaneous regulation of lipolysis, thermogenesis and oxidative metabolism. These data, together with the observation that TRIP-Br2 expression is selectively elevated in visceral fat in obese humans, suggests that this transcriptional co-regulator is a new therapeutic target for counteracting the development of obesity, insulin resistance and hyperlipidemia., Obesity and its related complications are associated with high morbidity and mortality, making it a pathologic condition of global importance (1), (2). Understanding the regulation of the factors that control [...]

BACKGROUND/OBJECTIVES: Previous studies have demonstrated the satiating properties of soups compared with solids; however, the mechanisms controlling soup-induced satiety are unknown. This study aimed to understand the physiological mechanisms causing soup to be more satiating. SUBJECTS/METHODS: A total of 12 volunteers were tested on three occasions after a solid meal, chunky soup or smooth soup test meal for gastric emptying (GE) using the sodium [1-[sup.13]C] acetate breath test, satiety using visual analog scales (VAS) and glycaemic response (GR) using finger prick blood samples. RESULTS: There was a significant difference in GE half-time (P = 0.022) and GE ascension time (P = 0.018), with the longest GE times for the smooth soup and the shortest for the solid meal. The GR area under the curve was significantly different between meals (P = 0.040). The smooth soup had the greatest GR (87.0 ± 49.5 mmol/l/min), followed by the chunky soup (65.4 ± 48.0 mmol/l/min), with the solid meal having the lowest GR (61.6 ± 36.8 mmol/l/min). Volunteers were fuller after the smooth soup compared with solid meal (P = 0.034). CONCLUSIONS: The smooth soup induced greater fullness compared with the solid meal because of a combination of delayed GE leading to feelings of gastric distension and rapid accessibility of nutrients causing a greater glycaemic response. European Journal of Clinical Nutrition (2013) 67, 8-11; doi: 10.1038/ejcn.2012.152; published online 24 October 2012 Keywords: physical state of food; satiety; gastric emptying; glycaemic response, INTRODUCTION Obesity and its related complications have become an overwhelming problem in our society. In 2009, obesity was estimated at ~23% among British adults, and with rates of obesity consistently [...]

Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletall muscle-specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance., Autophagy is an evolutionarily conserved process that delivers cytoplasmic constituents to lysosomes for degradation of aggregated proteins and recycling of organelles or nutrients (1). Autophagy is tightly controlled by amino [...]

Byline: Vinay. Kumar, Uma. Bhandari, Chakra. Tripathi, Geetika. Khanna Objective: Obesity plays a central role in the insulin resistance syndrome, which is associated with hyperinsulinemia, hypertension, hyperlipidemia, type 2 diabetes [...]

When you think of fat in the human body, you might picture a homogenous, white substance, much like a block of lard. But researchers are learning that the role of [...]

We show that high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing insulin signaling. Activation or overexpression of the IΚB kinase Β(IKKΒ) attenuated insulin signaling in cultured cells, whereas IKKΒ inhibition reversed insulin resistance. Thus, IKKΒ, rather than the cyciooxygenases, appears to be the relevant molecular target. Heterozygous deletion (Ikk[Beta.sup.+/-]) protected against the development of insulin resistance during high-fat feeding and in obese [Lep.sup.ob/ob] mice. These findings implicate an inflammatory process in the pathogenesis of insulin resistance in obesity and type 2 diabetes mellitus and identify the IKKΒ pathway as a target for insulin sensitization., Insulin resistance refers to a decreased capacity of circulating insulin to regulate nutrient metabolism. Individuals with insulin resistance are predisposed to developing type 2 diabetes, and insulin resistance is an [...]