新诊断老年2型糖尿病患者血清脂肪细胞型脂肪酸结合蛋白水平及意义

目的观察新诊断老年2型糖尿病(T2DM)患者血清脂肪细胞型脂肪酸结合蛋白(A-FABP)水平的变化及意义。方法通过比较72例新诊断T2DM患者与30例健康体检者(正常对照组)血糖、血脂、胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能指数(HOMA-β)及A-FABP等方面的差异,并分析A-FABP与血糖、血脂、HOMA-IR、HOMA-β的相关性。结果老年T2DM组体重指数(BMI)、空腹血糖(FPG)、餐后血糖(PPG)、糖化血红蛋白(Hb A1c)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、HOMA-IR和A-FABP显著高于正常对照组(P<0.05),而HOMA-β和高密度脂蛋白胆固醇(HDL-C)低于正常对照组(P<0.05),Pearson相关分析显示T2DM患者血清A-FABP与Hb A1c、PPG、TC、TG以及HOMA-IR呈正相关。结论老年T2DM患者血清A-FABP水平升高与胰岛素敏感性下降、糖脂代谢紊乱加重密切相关。     

中心性肥胖对老年新诊断2型糖尿病患者糖代谢及脂代谢的影响

目的探讨中心性肥胖对老年新诊断2型糖尿病患者血糖、血脂、游离脂肪酸（FFA）代谢以及胰岛素抵抗和胰岛β细胞分泌功能的影响。方法选取老年新诊断2型糖尿病患者90例,按照腰围（WC）（男性WC≥90cm,女性≥80cm）将所有研究对象分为中心性肥胖组和对照组,测定身高、体质量;所有研究对象均接受口服葡萄糖耐量实验（OGTT）,测定OGTT过程中0min、30min、60min、120min、180min的血糖、胰岛素（INS）、C肽（CP）、FFA水平,留取空腹血测定血脂全套,包括总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDLC）、低密度脂蛋白胆固醇（LDL-C）。采用HOMA-IR和HOMA-β分别评价胰岛素抵抗和胰岛β细胞分泌功能。比较2组之间上述指标的差异。结果老年新诊断2型糖尿病患者中心性肥胖组的空腹血糖、HOMA-IR、空腹FFA水平高于对照组（P〈0.05）。结论中心性肥胖对于老年新诊断2型糖尿病患者的糖代谢及脂代谢有影响,中心性肥胖者血糖水平高、血脂代谢紊乱,胰岛素抵抗严重。     

胰岛素泵强化治疗对新诊断2型糖尿病患者血糖及胰岛β细胞功能的影响

选取2017年1月至2019年1月的新诊断2型糖尿病患者102例,随机平分为对照组采用间断皮下注射胰岛素方法,观察组采用胰岛素泵持续注射胰岛素方法,3个月。结果:治疗后,两组空腹血糖(FPG)、餐后2h血糖(2hPBG)、胰岛素抵抗指数(HOMA-IR)均低于治疗前,胰岛素β细胞指数(HOMA-β)均高于治疗前,观察组较变化幅度大,(P 0. 05)。结论:胰岛素泵强化治疗能降低新诊断2型糖尿病患者血糖水平,改善胰岛β细胞功能。     

不同病程初发2型糖尿病对胰岛素短期强化治疗的反应

目的糖尿病初期胰岛素强化治疗可改善胰岛β细胞功能,但治疗时机尚无一致意见。本研究分析了不同病程初发2型糖尿病患者短期胰岛素强化治疗的胰岛β细胞功能改善程度。方法对2007年2月以来我科诊治的空腹血糖≥11.1mmol/L的初发2型糖尿病患者91例进行胰岛素强化治疗,对糖尿病病程在1周内组(A组,n=41)和12周以上组(B组,n=29)的患者进行分析总结。患者均行口服糖耐量试验测血糖和胰岛素、糖化血红蛋白(HbA1c)、糖化血清蛋白、血脂、尿酸、肝肾功能。每日4次三短一中胰岛素强化治疗4周后复测上述指标。采用稳态模型(HOMA)计算胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-β)。结果 A组和B组患者治疗后与治疗前相比,空腹血糖、糖化血清蛋白、HbA1c、甘油三酯、胆固醇、低密度脂蛋白胆固醇、收缩压和舒张压均有明显下降(P0.05),尿酸水平有所上升(P0.05),但两组相比无差异。两组患者强化治疗4周后HOMA-IR较治疗前无差异,而HOMA-β较治疗前有明显改善(P0.05),A组HOMA-β改善程度好于B组(P0.05)。以强化4周后HOMA-β为因变量,进行多因素回归分析,影响因素有体重指数、血压、甘油三酯水平、血糖达标时间、治疗前后HbA1c和糖化血清蛋白差值。结论糖尿病病程1周内进行强化治疗,胰岛β细胞功能改善好于病程12周以上,说明病程越短治疗效果越好。     

甘舒霖40R强化治疗对初诊2型糖尿病患者胰岛功能及胰岛素抵抗的影响

对32例初诊2型糖尿病患者进行每日2次甘舒霖40R胰岛素强化治疗12周,测定空腹血糖(FPG)、空腹胰岛素(FIns)及糖化血红蛋白(Hb A1c),计算稳态模型法β细胞功能指数(HOMA-β)、胰岛素抵抗指数(HOMA-IR)以及定量胰岛素敏感性指数(QUICKI)。结果治疗后,患者HOMA-β及QUICKI均升高(P 0. 001及P 0. 05); FIns,HOMA-IR,FPG,Hb A1c均下降(均P 0. 001)。结论:短期甘舒霖40R强化治疗能够改善初诊2型糖尿病患者胰岛β细胞功能,减轻IR,降糖效果确切。     

伴腹型肥胖的2型糖尿病患者的临床特点分析

目的:探讨伴腹型肥胖的2型糖尿病(T2DM)患者的临床特点。方法:选取T2DM住院患者171例,按腰围分为腹型肥胖组(AO组,男性>90 cm,女性>85 cm)和非腹型肥胖组(NAO组,男性≤90 cm,女≤85 cm),比较各组的糖代谢、脂代谢、新稳态模型(HOMA2)胰岛B细胞分泌指数(HOMA2-B)和胰岛素敏感性指数(HOMA2-S)。结果:AO组血压、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、C反应蛋白(CRP)、血糖和C肽(CP0、CP30、CP120)均较NAO组显著升高,而高密度脂蛋白胆固醇(HDL-C)、HOMA2-S则明显降低。结论:伴腹型肥胖的T2DM患者多伴TG水平升高,且血糖失控和胰岛素抵抗程度更重。     

血清脂肪因子与代谢综合征的关系

121例代谢综合征(MS)患者和120名对照者入选本研究以探讨血清脂肪因子与MS的关系.对照组、非腹型肥胖MS组及腹型肥胖MS组的血清抵抗素和脂肪细胞型脂肪酸结合蛋白(A-FABP)依次增高,而脂联素水平依次降低(均P<0.05).MS组抵抗素与体重指数(BMI)、腰围、收缩压、空腹血糖和A-FABP呈正相关(P<0.05或P<0.01);脂联素与高密度脂蛋白胆固醇呈正相关,而与BMI、腰围、空腹胰岛素、甘油三酯、稳态模型评估的胰岛素抵抗指数(HOMA-IR)呈负相关.     

妊娠糖尿病患者血清脂肪细胞型脂肪酸结合蛋白与胰岛素抵抗的关系探讨

目的 探讨孕期血清脂肪细胞型脂肪酸结合蛋白(A-FABP)水平变化与妊娠期糖尿病胰岛素抵抗的关系.方法 96例孕妇,根据75 g葡萄糖耐量试验(OGTT)结果 分A-FABP为正常葡萄糖耐量妊娠组(NGT组)和妊娠期糖尿病组(GDM组).用ELISA方法 测定患者血清A-FABP浓度,同时测定患者身高、体重,计算体重指数(BMI),化验血糖、血脂、空腹胰岛素,计算稳态模型胰岛素抵抗指数(HOMA - IR)和胰岛素敏感性指数( ISI),分析各指标与A-FABP的关系.结果 GDM组血清A-FABP、三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、空腹血糖(FPG)、餐后2 h血糖(2 hPG)、空腹胰岛素(FINS)、HOMA -IR均高于NGT组,而ISI低于NGT组,差异有统计学意义(P<0.05).多元线性回归分析表明,A-FABP与 BMI(β=0.186,P=0.027)、TG(β=0.182,P=0.024)、HOMA -IR(β=0.214,P=0.014)呈正相关,与ISI成负相关(β=-0.212,P=0.014).结论 GDM 患者血清A-FABP水平明显升高,并与胰岛素抵抗密切相关.     

利拉鲁肽联合二甲双胍对肥胖型2型糖尿病患者胰岛β细胞功能的影响

选取2016年5月到2018年5月肥胖型2型糖尿病患者96例,随机平分成对照组给予二甲双胍,观察组接受利拉鲁肽联合二甲双胍治疗。结果观察组治疗后三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、血清总胆固醇(TC)、稳态模型胰岛素抵抗指数(HOMA-IR)低于对照组,胰岛β细胞分泌指数(HOMA-β)高于对照组,(P 0. 05)。结论利拉鲁肽与二甲双胍联合治疗肥胖型2型糖尿病患者可有效改善胰岛β细胞功能,降低血脂水平。     

短期胰岛素泵强化治疗对初诊2型糖尿病患者胰岛β细胞功能及血脂代谢的影响

观察短期胰岛素泵强化治疗对初诊2型糖尿病患者的胰岛β细胞功能及血脂代谢的影响。方法新诊断的2型糖尿病患者57例,给予为期2周的胰岛素泵强化治疗,治疗前后行口服葡萄糖耐量试验(OGTT)、胰岛素释放试验(OGIRT)、糖化血红蛋白(HbA1c)检测;对糖脂控制情况、空腹胰岛素浓度(FIns)、胰岛素曲线下面积(AUC)、胰岛β细胞功能指数(HOMA-β)、胰岛素抵抗指数(HOMA-IR)、早时相胰岛素分泌指数(I30/G30)进行比较。结果经2周胰岛素泵强化治疗后,患者空腹血糖(FPG)、餐后2h血糖(2hPG)、HOMA-IR、血清总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-c)、甘油三酯(TG)均较治疗前明显降低,空腹胰岛素浓度、胰岛素曲线下面积、I30/G30、HOMA-β、高密度脂蛋白胆固醇(HDL-c)明显升高。结论初诊2型糖尿病短期应用胰岛素泵治疗能早期解除糖脂毒性,显著改善糖脂代谢及胰岛β细胞功能,减轻胰岛素抵抗。     

Oestrogen alters adipocyte biology and protects female mice from adipocyte inflammation and insulin resistance

Aims: Obesity is associated with insulin resistance, liver steatosis and low‐grade inflammation. The role of oestrogen in sex differences in the above co‐morbidities is not fully understood. Our aim was to assess the role oestrogen has in modulating adipocyte size, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis. Methods: To determine the role oestrogen has in the above co‐morbidities related to obesity, we randomized C57BL/6J mice into four groups (15 mice per group): (i) male, (ii) non‐ovariectomized female (novx), (iii) ovariectomized female (ovx) and (iv) ovariectomized female mice supplemented with 17β estradiol (ovx‐E). Mice received either a low‐fat (LF) or a high‐fat (HF) diet for 10 weeks. Outcomes measured were bodyweight, body fat, adipocyte diameter, adipose tissue lipolysis markers, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis. Results: Male and ovx‐female mice consuming the HF diet had a higher propensity of gaining weight, specifically in the form of body fat. Oestrogen protected female mice from adipocyte hypertrophy and from developing adipose tissue oxidative stress and inflammation. Moreover, novx‐female and ovx‐female+E mice had higher phosphorylated levels of protein kinase A and hormone sensitive lipase, markers associated with lipolysis. Additionally, male and ovx female mice had a higher propensity of developing liver steatosis and insulin resistance. In contrast, oestrogen protected female mice from developing liver steatosis and from becoming insulin resistant. Conclusion: We show that oestrogen protects female mice from adipocyte hypertrophy and adipose tissue oxidative stress and inflammation. Furthermore, oestrogen prevented female mice from developing liver steatosis and from becoming insulin resistant.     

Adipose tissue and adipocyte dysregulation

Obesity-associated insulin resistance is a complex disorder involving a number of candidate molecules, pathways and transduction systems possessing potential causal actions. Inflammation in adipose tissue (AT) is one mechanism proposed to explain the development of insulin resistance, while identification of factors that lead to or cause AT dysfunction when it reaches its limit of expansion represents an important challenge. Pathological expansion of AT is characterized by changes in its blood flow, and the presence of enlarged and dysfunctional adipocytes that begin an inflammatory campaign of altered adipokine and cytokine secretions. Adipocyte senescence, necrosis and death are associated with increased immune cell and macrophage infiltration of AT in obesity. This can boost inflammation and reinforce fat cell dysfunction and death. In addition, pathological fat mass expansion is also related to limited recruitment of fat cell progenitors able to proliferate and differentiate into healthy small fat cells to compensate for cell death and preserve adipocyte numbers. Limiting vascular development and enhancing fibrotic processes worsen inflammation towards chronic irreversibility. The AT expandability hypothesis states that failure of AT expansion is one of the key factors linking positive energy balance and cardiometabolic risks, not obesity per se. Besides the usual treatment of obesity based on behavioral approaches (specific dietary/nutritional approaches together with increased physical activity), a number of questions remain concerning the possible recovery of metabolic health after inflammation-preventing interventions.     

Determinants of brown adipocyte development and thermogenesis

The brown adipocyte is a thermogenic cell. Its thermogenic potential is conferred by uncoupling protein-1, which 'uncouples' adenosine triphosphate synthesis from energy substrate oxidation. Brown fat cells in so-called classical brown adipose tissue (BAT) share their origin with myogenic factor-5-expressing myoblasts. The development of myocyte/brown adipocyte progenitor cells into a brown adipocyte lineage is apparently triggered by bone morphogenetic protein-7, which stimulates inducers of brown fat cell differentiation, such as PRD1-BF1-RIZ1 homologous domain-containing-16 and peroxisome proliferator-activated receptor-γ co-activator-1-α. The control of brown fat cell development and activity is physiologically ensured by the sympathetic nervous system (SNS), which densely innervates BAT. SNS-mediated thermogenesis is largely governed by hypothalamic and brainstem neurons. With regard to energy balance, the leptin-melanocortin pathway appears to be a major factor in controlling brown adipocyte thermogenesis. The involvement of this homeostatic pathway further supports the role of the brown adipocyte in energy balance regulation. The interest for the brown fat cell and its potential role in energy balance has been further rejuvenated recently by the demonstration that BAT can be present in substantial amounts in humans, in contrast to what has always been thought. Positron emission tomography/computed tomography scanning investigations have indeed revealed the presence in humans of important neck and shoulder cold-activable BAT depots, in particular, in young, lean and female subjects. This short review summarizes recent progress made in the biology of the brown fat cell and focuses on the determinants of the brown adipocyte development and activity.