血清生长激素水平与儿童单纯性肥胖伴身高略矮的关系

目的:探讨血清生长激素(growth hormone,GH)水平与儿童单纯性肥胖伴身高略矮的关系。方法:选择2013年1月~2013年11月27例在我院儿童保健科门诊就诊的被诊断为单纯性肥胖症的儿童,且其身高均小于同龄儿童平均身高5 cm以上,采用放射免疫法检测其血清生长激素水平,分析其生长激素水平的变化及其意义。结果:27例患儿化验结果显示生长激素完全缺乏者22例,部分缺乏5例。结论:生长激素缺乏可能是肥胖伴身高略矮儿童患肥胖症的重要原因,测定血清生长激素水平有助于了解肥胖伴身高略矮儿童体内生长激素水平从而应用于肥胖症的病因治疗。     

Glucocorticoids decrease serum adiponectin level and WAT adiponectin mRNA expression in rats

Objective

Accumulating evidence suggests that adiponectin plays an important role in the genesis of obesity and insulin resistance. Although it has been shown that glucocortocoids (GC) inhibit adiponectin expression in vitro, there exist discrepant results in vivo. In this study, we observe the effect of GC on the serum adiponectin level and adiponectin expression in white adipose tissue (WAT) in male SD rats.

Methods

An obese rat model was made by a high-fat diet. Both non-obese and obese rats were randomly divided into normal saline (intraperitoneal injection with normal saline 0.2 ml/100 g day for 20 days, NS), a low dose GC group (intraperitoneal injection with hydrocortisone sodium succinate 5 mg/kg day for 20 days, LDG) and a high dose GC group, respectively (intraperitoneal injection with hydrocortisone sodium succinate 15 mg/kg day for 20 days, HDG). Serum adiponectin levels were detected by ELISA and the adiponectin mRNA level was assayed by Northern blot.

Results

The serum adiponectin level significantly decreased after 80 days of the high-fat diet (P < 0.05), while it was not decreased after 80 days of the chow diet (P > 0.05). The serum adioponectin levels in both the non-obese and obese rats were significantly decreased after a 20-day GC injection period (P < 0.01). The adiponectin mRNA levels in epididymal fat after high dose GC injection, in both non-obese and obese rats were also decreased (P < 0.001).

Conclusions

A high-fat diet decreased serum adiponectin levels in the rat. GC decreased serum adiponectin levels, and this might be due to inhibited adiponectin mRNA expression in WAT. High-fat diet and GC have a synergistic effect on inhibiting adiponectin expression in rats.     

大口鲶ob基因的克隆及其在毕赤酵母中的表达

1994年Zhang等人利用定位克隆技术首次成功地克隆出小鼠肥胖基因(obese gene,ob基因)及人类同源序列后[1],其他动物如鸡、鸭、猪等的肥胖基因结构和部分功能相继得到了报道,但关于鱼类ob基因的结构和功能研究报道较少.     

Nitric oxide concentrations in gas emanating from the tails of obese rats

Abstract

This study was undertaken to investigate the effects of oral L-arginine administration and exercising training on the NO concentration emanating from rat tail and NO_x in plasma. Obese (fa/fa) Zucker rats (n = 22) were divided into four groups: (1) oral L-arginine administration (A) (n = 6), (2) exercise training (E), (3) exercise training + L-arginine administration (E + A) (n = 5), and (4) non-exercise training + non-L-arginine administration (N) (n = 6). The control (+/+) Zucker rats (n = 22) were also divided into the same four groups. The body weight of the E + A and the A groups was significantly lower than that of the N group. The NO concentration emitted from the tail was higher in the L-arginine (E + A and A) groups than in the non-L-arginine (E and N) groups in both obese and control rats. Exercise training did not affect the skin gas NO concentration in either obese or control rats. Plasma NO_x concentrations in four obese rats were significantly higher than those observed in control rats. Exercise training did not influence the level of plasma NO_x in obese or control rats. In conclusion, this study confirmed that L-arginine administration increases the skin gas NO concentration and obesity increases the plasma NO_x level. The plasma NO_x concentrations were not affected by L-arginine administration or exercise training in obese or control rats.     

Biased cellular locations of tandem repeat antigens in African trypanosomes

Objective

The adverse effects of metabolic disorders in obesity have been extensively studied; however, the pathologic effects of hyperphosphatemia or phosphate toxicity in obesity have not been studied in similar depth and detail, chiefly because such an association is thought to be uncommon. Studies have established that the incidence of obesity-associated nephropathy is increasing. Because hyperphosphatemia is a major consequence of renal impairment, this study determines the in vivo effects of hyperphosphatemia in obesity.

Methods and results

We genetically induced hyperphosphatemia in leptin-deficient obese (ob/ob) mice by generating ob/ob and klotho double knockout [ob/ob-klotho^−/−] mice. As a control, we made ob/ob mice with hypophosphatemia by generating ob/ob and 1-alpha hydroxylase double knockout [ob/ob-1α(OH)ase^−/−] mice. Compared to the wild-type mice, all three obese background mice, namely ob/ob, ob/ob-klotho^−/−, and ob/ob-1α(OH)ase^−/− mice developed hypercholesterolemia. In addition, the hyperphosphatemic, ob/ob-klotho^−/− genetic background induced generalized tissue atrophy and widespread soft-tissue and vascular calcifications, which led to a shorter lifespan; no such changes were observed in the hypophosphatemic, ob/ob-1α(OH)ase^−/− mice. Significantly, in contrast to the reduced survival of the ob/ob-klotho^−/− mice, lowering serum phosphate levels in ob/ob-1α(OH)ase^−/− mice showed no such compromised survival, despite both mice being hypercholesterolemic.

Conclusion

These genetic manipulation studies suggest phosphate toxicity is an important risk factor in obesity that can adversely affect survival.     

人ob基因克隆及其亚细胞定位的研究

目的:旨在克隆人肥胖(obese,ob)基因的全长cDNA序列,与EGFP重组构建融合蛋白表达载体,并分析其亚细胞水平的定位.方法:提取人脂肪细胞总RNA,采用RT-PCR方法扩增出人ob基因cDNA,并克隆至真核表达载体pEGFP-CI,重组质粒转染NIH-3T3细胞,荧光显微镜分析EGFP-ob融合蛋白的亚细胞定位.结果:克隆的ob基因cDNA为501bp,共编码167个氨基酸,与GenBank公布的人ob基因序列一致,荧光显微镜分析表明,重组的EGFP-ob融合蛋白主要分布于NIT-3T3的细胞质中.结论:成功克隆了人OB基因的cDNA序列,构建人OB基因的真核表达载体pEGFP-CI-ob,融合蛋白EGFP-ob定位于NIH-3T3细胞质中.     

黄连素对肥胖小鼠肠道菌群的影响及其机制

为了探索黄连素对肥胖小鼠肠道菌群的影响和作用机制,本研究将40只雄性昆明种小鼠随机分为空白组、模型组、黄连素高剂量组、黄连素中剂量组和黄连素低剂量组,每组8只,除空白组外,其余4组给予高脂饮食,建立实验性肥胖小鼠模型。造模14 d后,全部给予正常饮食,黄连素高、中、低剂量组灌胃给予每天0.1～0.3 mL/10 g的药物干预,空白组和模型组给予等剂量的生理盐水,给药持续14 d。每周称量两次体质量,并分别于实验第0、14、28天从眼眶取血测定血脂和炎性因子的含量,收集小鼠粪便测定乳酸杆菌和双歧杆菌的数量。研究结果表明:空白组和模型组小鼠的体质量在第14天时有明显差异,造模成功;实验第28天,黄连素各给药组小鼠的体质量与模型组相比有显著性差异。模型组双歧杆菌、乳酸菌的数量和血脂水平与空白组比较有显著性差异,黄连素给药组能显著改善肥胖小鼠的血脂水平和双歧杆菌、乳酸杆菌的数量。本研究结果初步得出结论认为:黄连素改善肥胖小鼠的作用机制可能与脂质代谢、炎性反应和肠道微环境的改变密切相关。     

8周有氧运动对肥胖大鼠消化道嗜银 细胞形态及分布密度的影响

为了研究有氧运动对肥胖大鼠（Rattus norvegicus）消化道嗜银细胞形态及分布密度的影响,本实验采用Grimelius银染法观察8周运动组（n = 9）与对照组（n = 9）肥胖大鼠消化道嗜银细胞形态及分布密度。结果显示,大鼠消化道各部位均有嗜银细胞分布;两组大鼠消化道嗜银细胞形态上无差异,均以圆形、椭圆形、锥体形、梭形为主;两组大鼠消化道嗜银细胞分布密度高峰均位于胃体,而低谷有所不同,对照组大鼠消化道嗜银细胞的分布密度低谷位于食管、贲门,运动组大鼠位于食管、贲门、空肠、回肠、直肠;两组相比,食管和直肠两部位分布密度差异不显著（P > 0.05）,其余各部位均有差异,且运动组大鼠贲门、胃体、盲肠、结肠嗜银细胞分布密度极显著低于对照组（P < 0.01）,幽门、空肠嗜银细胞分布密度极显著高于对照组（P < 0.01）,运动组十二指肠、回肠嗜银细胞分布密度显著高于对照组（P < 0.05）。两组动物嗜银细胞分泌密度的这种改变与动物机体所处不同生理状态以及消化道各部位功能有关。     

肥胖2型糖尿病患者神经肽Y水平与糖脂代谢的相关性分析

目的:探讨肥胖2型糖尿病患者神经肽Y(NPY)水平与糖脂代谢的相关性。方法:选择2017年7月至2019年7月我院接诊的134例肥胖2型糖尿病患者为本研究对象,设为观察组,并选择我院收治的2型糖尿病非肥胖患者100例作为对照组,分析腰围、腹围、臀围、BMI、腰臀比(WHR)、血清NPY、空腹血糖(FPG)、糖化血红蛋白(Hb Alc)、空腹胰岛素(FINS)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平变化情况,及其之间的相关性分析。结果:观察组腹围、腰围、臀围、腰臀比及BMI水平均显著高于对照组,差异显著(P0.05);观察组患者血清NPY、FPG、Hb Alc水平显著高于对照组,FINS水平显著低于对照组,差异显著(P0.05);观察组患者血清TC、TG、LDL-C水平显著高于对照组,HDL-C水平显著低于对照组,差异显著(P0.05);将FPG、Hb Alc、FINS、TC、TG、LDL-C、HDL-C作为因变量,将血清NPY作为自变量,在相关性分析结果中显示,血清NPY和FPG、Hb Alc、TC、TG、LDL-C之间均呈正相关(r=0.399,0.173,0.435,0.451,0.376,P均0.05),血清NPY和FINS、HDL-C之间均呈负相关(r=-0.566,-0.223,P均0.05)。结论:在肥胖2型糖尿病患者中NPY水平显著升高,且与腹部脂肪增加、糖脂代谢显著相关。     

Optimization of condition(s) towards establishment of primary islet cell cultures from WNIN/Ob mutant rat

WNIN/Ob, a mutant rat strain, developed at the National Center for Laboratory Animal Sciences (NCLAS) facility of National Institute of Nutrition (NIN), is a new animal model to study the metabolic syndrome. These animals have 47% fat in their body and isolation of islets from these animals were compounded due to the formation of amorphous viscous and jelly like material which reduced the islet yield. However, islets isolated from WNIN adult (≥12 months) control rats gave a good islet recovery, under standard isolation procedures using collagenase digestion. In the present study we optimized culture conditions in WNIN/Ob rats to isolate islets with higher yield, and also established primary islet cell cultures from these mutant rats, retaining cellular integrity and functionality.