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Lipid accumulation in overweight type 2 diabetic subjects: Relationships with insulin sensitivity and adipokines

机译:超重2型糖尿病受试者中的脂质蓄积:与胰岛素敏感性和脂肪因子的关系

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摘要

Adipokines are known to play a fundamental role in the etiology of obesity, that is, in the impaired balance between increased feeding and decreased energy expenditure. While the adipokine-induced changes of insulin resistance in obese diabetic and nondiabetic subjects are well known, the possible role of fat source in modulating insulin sensitivity (IS) remains controversial. The aim of our study was to explore in overweight type 2 diabetic patients (T2DM) with metabolic syndrome IS in different energy storage conditions (basal and dynamic) for relating it to leptin and adiponectin. Sixteen T2DM (5/11 F/M; 59 ± 2 years; 29.5 ± 1.1 kg/m2) and 16 control (CNT 5/11; 54 ± 2; 29.1 ± 1.0) underwent an oral glucose tolerance test. Fasting IS was measured by QUICKI, while the dynamic one with OGIS. The insulinogenic index (IGI) described beta cell function. Also, the lipid accumulation product parameter (LAP) was assessed. LAP accounts for visceral abdominal fat and triglycerides, and it is known to be related to IS. Possible interrelationships between LAP and adipokines were explored. In T2DM and CNT, adiponectin (7.4 ± 0.5 vs. 7.8 ± 0.9 μg/mL), leptin (13.3 ± 3.0 vs. 12.4 ± 2.6 ng/mL), and QUICKI (0.33 ± 0.01 vs. 0.33 ± 0.01) were not different (P 0.40), at variance with OGIS (317 ± 11 vs. 406 ± 13 mL/min/m2; P = 0.006) and IGI (0.029 ± 0.005 vs. 0.185 ± 0.029 × 103 pmolI/mmolG; P = 0.00001). LAP was 85 ± 15 cm × mg/dL in T2DM and 74 ± 10 in CNT (P 0.1), correlated with OGIS in all subjects (R = -0.42, P = 0.02) and QUICKI (R = -0.56, P = 0.025) in T2DM. Leptin correlated with QUICKI (R = -0.45, P = 0.009), and adiponectin correlated with OGIS (R = 0.43, P = 0.015). In overweight T2DM, insulin sensitivity in basal condition appears to be multifaceted with respect to the dynamic one, because it should be more fat-related. Insulin sensitivity appears to be incompletely described by functions of fasting glucose and insulin values alone and the use of other indices, such as LAP could be suggested.
机译:已知脂肪因子在肥胖的病因中起着基本作用,即在增加的进食和减少的能量消耗之间的平衡受损。尽管肥胖和非糖尿病患者中脂肪因子诱导的胰岛素抵抗变化是众所周知的,但脂肪来源在调节胰岛素敏感性(IS)中的可能作用仍存在争议。我们研究的目的是探索在不同能量存储条件(基础和动态)下患有代谢综合征IS的超重2型糖尿病患者(T2DM)与瘦素和脂联素的关系。进行了16例T2DM(5/11 F / M; 59±2年; 29.5±1.1 kg / m2)和16例对照(CNT 5/11; 54±2; 29.1±1.0)进行了口服葡萄糖耐量试验。禁食IS由QUICKI衡量,而动态IS由OGIS衡量。胰岛素生成指数(IGI)描述了β细胞的功能。此外,评估了脂质堆积产物参数(LAP)。 LAP占内脏腹部脂肪和甘油三酸酯,并且已知与IS有关。探讨了LAP与脂肪因子之间可能存在的相互关系。在T2DM和CNT中,脂联素(7.4±0.5 vs. 7.8±0.9μg/ mL),瘦素(13.3±3.0 vs. 12.4±2.6 ng / mL)和QUICKI(0.33±0.01 vs. 0.33±0.01)没有差异(P> 0.40),与OGIS(317±11 vs. 406±13 mL / min / m2; P = 0.006)和IGI(0.029±0.005 vs.0.185±0.029×103 pmolI / mmolG; P = 0.00001)有所不同。 T2DM中LAP为85±15 cm×mg / dL,而CNT中LAP为74±10(P> 0.1),与所有受试者的OGIS(R = -0.42,P = 0.02)和QUICKI(R = -0.56,P = T2DM中的0.025)。瘦素与QUICKI相关(R = -0.45,P = 0.009),脂联素与OGIS相关(R = 0.43,P = 0.015)。在超重的T2DM中,基本情况下的胰岛素敏感性相对于动态中的胰岛素敏感性似乎是多方面的,因为它应该与脂肪更多相关。仅通过禁食葡萄糖和胰岛素值的功能似乎无法完全描述胰岛素敏感性,并且可能建议使用其他指标,例如LAP。

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