Adaptive Thermogenesis in Mice Is Enhanced by Opsin 3-Dependent Adipocyte Light Sensing

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Cbx4 Sumoylates Prdm16 to Regulate Adipose Tissue Thermogenesis

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Resistance to Aging-Associated Obesity in Capsaicin-Desensitized Rats One Year after Treatment

Previous studies demonstrated reduced weight of abdominal white adipose tissue depots and of carcass fat in capsaicin-desensitized (Cap-Des) rats up to 8 months after treatment. The objective of the present study was to find out whether aging-associated obesity and hyperplasia of retroperitoneal white adipose tissue was prevented in older (13.5 month old) Cap-Des rats, one year after treatment with Cap (done when they were 1.5 months old). The prevalence of obesity is known to increase in rats by this age. Abdominal white adipose tissue depots weighed less in old Cap-Des rats, both epididymal (9% less) and retroperitoneal (30% less). The number of mature white adipocytes was 28% less in the retroperitoneal depot but was not significantly different in the epididymal depot. Adipocyte size was not different. Carcass fat was less, both total and as percent of body weight. Food intake was normal for their reduced body size. The exponential increase in retroperitoneal white adipose tissue weight characteristic of aging rats that are becoming obese was virtually absent in Cap-Des rats. We conclude that lack of function of capsaicin-sensitive afferent autonomic nerves, known to be destroyed in Cap-Des rats, results in an alteration in energy balance conducive to leanness. We suggest that the attenuated age-associated increase in circulating CGRP (derived mainly from capsaicin-sensitive nerves) in the Cap-Des rat results in a lower degree of aging-associated insulin-resistance, hence in a lesser degree of obesity.     

转录辅助活化因子PGC-1家族的生物学特性及功能

过氧化物酶体增殖物激活受体γ辅助活化因子1(PGC-1)家族共有PGC-1α,PGC-1β和PRC(PGC-1相关因子)3个成员,该家族在机体诸多代谢过程中发挥重要作用,包括调节机体适应性产热、线粒体的生成、脂质代谢、调节血糖平衡及葡萄糖转运、激活糖异生的关键酶和影响肌纤维类型的转换等.成员间功能也存在差异,PGC-1α的上述功能表现的较为明显,而PGC-1β在调节脂肪细胞分化及脂类代谢中具有独特的功能,PRC则仅发现其在调节线粒体的生物合成及细胞增殖中有作用.研究认为,通过调节PGC-1家族的生理功能,可治疗肥胖及糖尿病等疾病,尤其PGC-1β可作为改善机体胰岛素抵抗的新药物靶点.本文就PGC-1家族的特征、生理功能及相互作用研究进行简要综述.     

Effects of photoperiod on energy budgets and thermogenesis in Mongolian gerbils (Meriones unguiculatus)

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To investigate the role of photoperiod on the regulation of energy budgets and thermogenesis in Mongolian gerbils, body mass (BM), body fat mass (BFM), basal metabolic rate (BMR), nonshivering thermogenesis (NST), gross energy intake (GEI), mitochondrial cytochrome c oxidase (COX) activity and uncoupling protein1 (UCP1) content of brown adipose tissue (BAT), and serum tri-iodothyronine (T₃), thyroxine (T₄) and leptin levels were measured.     

Acute and chronic cold exposure differentially affects the browning of porcine white adipose tissue

Piglets are characteristically cold intolerant and thus susceptible to high mortality. However, browning of white adipose tissue (WAT) can induce non-shivering thermogenesis as a potential strategy to facilitate the animal’s response to cold. Whether cold exposure can induce browning of subcutaneous WAT (sWAT) in piglets in a similar manner as it can in humans remains largely unknown. In this study, piglets were exposed to acute cold (4°C, 10 h) or chronic cold exposure (8°C, 15 days), and the genes and proteins of uncoupling protein 1 (UCP1)-dependent and independent thermogenesis, mitochondrial biogenesis, lipogenic and lipolytic processes were analysed. Interestingly, acute cold exposure induced browning of porcine sWAT, smaller adipocytes and the upregulated expression of UCP1, PGC1α, PGC1β, C/EBPβ, Cidea, UCP3, CKMT1 and PM20D1. Conversely, chronic cold exposure impaired the browning process, reduced mitochondrial numbers and the expression of browning markers, including UCP1, PGC1α and PRDM16. The present study demonstrated that acute cold exposure (but not chronic cold exposure) induces porcine sWAT browning. Thus, browning of porcine sWAT could be a novel strategy to balance the body temperature of piglets, and thus could be protective against cold exposure.     

Immobilized Aminoacylase on Porous Glass Beads

The preparation and properties of immobilized aminoacylase on porous glass by covalent binding [Porous glass-CVB-aminoacylase] and the continuous enzymatic reactions using such preparations are described.

Two types of porous glass-CVB-aminoacylase were prepared. One was aminoacylase covalently bound to alkylaminosilane derivative of porous glass with glutaraldehyde as a coupling agent [Alkylamino-porous glass-CVB-aminoacylase], and the other was aminoacylase covalently bound to arylaminosilane derivative of porous glass with nitrous acid as a coupling agent [Arylamino-porous glass-CVB-aminoacylase]. The enzyme activities of such immobilized aminoacylases were 3.2~13.0 units/ml glass for the former and 1.9~6.8 units/ml glass for the latter. Especially, alkylamino porous glass-CVB-aminoacylase showed excellent stability at pH 6~9 and temperature below 50°C, and was able to be stored for more than six months without appreciable loss of the activity.

The continuous enzyme reaction using the alkylamino porous glass-CVB-aminoacylase packed in a column was operated for 54 days at 37°C, and the half-life of the immobilized enzyme was calculated to be 78 days. From these results, it was recognized that such an immobilized aminoacylase on porous glass would be applicable in an industrial preparation of various l-amino acids from their dl-forms.     

Mitochondrial Proton Leak and the Uncoupling Proteins

An energetically significant leak of protons occurs across the mitochondrial inner membranesof eukaryotic cells. This seemingly wasteful proton leak accounts for at least 20% of thestandard metabolic rate of a rat. There is evidence that it makes a similar contribution tostandard metabolic rate in a lizard. Proton conductance of the mitochondrial inner membranecan be considered as having two components: a basal component present in all mitochondria,and an augmentative component, which may occur in tissues of mammals and perhaps ofsome other animals. The uncoupling protein of brown adipose tissue, UCP1, is a clear exampleof such an augmentative component. The newly discovered UCP1 homologs, UCP2, UCP3,and brain mitochondrial carrier protein 1 (BMCP1) may participate in the augmentativecomponent of proton leak. However, they do not appear to catalyze the basal leak, as this isobserved in mitochondria from cells which apparently lack these proteins. Whereas UCP1plays an important role in thermogenesis, the evidence that UCP2 and UCP3 do likewiseremains equivocal.     

Taking control over intracellular fatty acid levels is essential for the analysis of thermogenic function in cultured primary brown and brite/beige adipocytes

Thermogenesis in brown adipocytes, conferred by mitochondrial uncoupling protein 1 (UCP1), is receiving great attention because metabolically active brown adipose tissue may protect humans from metabolic diseases. In particular, the thermogenic function of brown‐like adipocytes in white adipose tissue, known as brite (or beige) adipocytes, is currently of prime interest. A valid procedure to quantify the specific contribution of UCP1 to thermogenesis is thus of vital importance. Adrenergic stimulation of lipolysis is a common way to activate UCP1. We here report, however, that in this frequently applied setup, taking control over intracellular fatty acid levels is essential for the analysis of thermogenic function in cultured brown and brite adipocytes. By the application of these findings, we demonstrate that UCP1 is functionally thermogenic in intact brite adipocytes and adrenergic UCP1 activation is largely dependent on adipose triglyceride lipase (ATGL) rather than hormone sensitive lipase (HSL).