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1.
Anthropomorphic measures among type 1 diabetic patients are changing as the obesity epidemic continues. Excess fat mass may impact bone density and ultimately fracture risk. We studied the interaction between bone and adipose tissue in type 1 diabetes subjects submitted to two different clinical managements: (I) conventional insulin therapy or (II) autologous nonmyeloablative hematopoietic stem-cell transplantation (AHST). The study comprised 3 groups matched by age, gender, height and weight: control (C = 24), type 1 diabetes (T1D = 23) and type 1 diabetes treated with AHST (T1D-AHST = 9). Bone mineral density (BMD) and trabecular bone score (TBS) were assessed by dual X-ray absorptiometry (DXA). 1H Magnetic resonance spectroscopy was used to assess bone marrow adipose tissue (BMAT) in the L3 vertebra, and abdominal magnetic resonance imaging was used to assess intrahepatic lipids (IHL), visceral (VAT) and subcutaneous adipose tissue (SAT). Individuals conventionally treated for T1D were more likely to be overweight (C = 23.8 ± 3.7; T1D = 25.3 ± 3.4; T1D-AHST = 22.5 ± 2.2 Kg/m2; p > 0.05), but there was no excessive lipid accumulation in VAT or liver. Areal BMD of the three groups were similar at all sites; lumbar spine TBS (L3) was lower in type 1 diabetes (p < 0.05). Neither SAT nor VAT had any association with bone parameters. Bone marrow adipose tissue (BMAT) lipid profiles were similar among groups. BMAT saturated lipids were associated with cholesterol, whereas unsaturated lipids had an association with IGF1. Overweight and normal weight subjects with type 1 diabetes have normal areal bone density, but lower trabecular bone scores. Adipose distribution is normal and BMAT volume is similar to controls, irrespective of clinical treatment.  相似文献   
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Pemphigus vulgaris (PV) is a chronic autoimmune disorder with potentially fatal outcomes. The aim of this study was to investigate the effect of l ‐carnitine (LC) on secreted frizzled‐related protein‐5 (SFRP5), omentin, visfatin, and glycemic indices in PV patients under corticosteroid treatment. In this randomized, double‐blind, placebo‐controlled clinical trial, 52 patients with PV were divided randomly into two groups to receive 2 g of LC or a placebo for 8 weeks. Serum levels of SFRP5, omentin, visfatin, and also glycemic indices were evaluated at the baseline and end of the study. LC supplementation significantly decreased the serum level of visfatin (95% CI [?14.718, ?0.877], p = .05) and increased the serum levels of SFRP5 (95%CI [1.637, 11.380], p < .006) and omentin (95% CI [9.014, 65.286], p < .01). However, LC supplementation had no significant effects on the serum levels of glycemic factors such as insulin (95% CI [?1.125, 3.056], p = .426), fasting blood sugar (95% CI [?4.743, 3.642], p = .894), homeostatic model assessment of insulin resistance (95% CI [?0.305, 0.528], p = .729), and quantitative insulin‐sensitivity check index (95% CI [?0.016, ?0.010], p = .81). LC supplementation decreased visfatin serum level and increased omentin‐1 and SFRP5 serum levels in patients with PV. However, it has no significant effect on the serum levels of insulin and glycemic indices.  相似文献   
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目的:探讨妊娠期糖尿病(GDM)患者血清脂肪因子omentin-1、chemerin水平变化及与GDM糖脂代谢、炎症指标等的相关性。方法 ELISA法定量85例GDM及匹配设置的85例糖耐量正常孕妇(NGT)血清omentin-1及chemerin水平,同时检测两组糖脂生化指标、炎症指标、空腹胰岛素(FINS)水平,计算胰岛素抵抗指数(HOMA-IR)。以单因素相关分析、多元逐步回归分析处理。结果(1)GDM组孕前BMI、hs-CRP、血脂、血糖、FINS、HOMA-IR、血清chemerin均明显高于NGT组,血清omentin-1明显低于NGT组(P<0.05);(2)血清omentin-1:肥胖GDM<非肥胖GDM≈肥胖NGT<非肥胖NGT(P<0.05);血清chemerin:肥胖GDM>非肥胖GDM≈肥胖NGT>非肥胖NGT(P<0.05);(3)析因分析,产前肥胖和/或HOMA-IR≥2时,血清omentin-1水平明显降低;产前肥胖血清chemerin明显升高,但与HOMA-IR≥2无关联;(4)相关性分析:血清omentin-1与HDL明显正相关,而与孕前BMI、产前BMI、FPG、FINS及HOMA-IR明显负相关;chemerin与TC、TG、hs-CRP及FPG明显正相关;omentin-1和chemerin之间无明显相关性(P=0.301);(5)孕前BMI、TG、FPG、FINS是GDM血清omentin-1的独立影响因素;TG、LDL、hs-CRP是GDM血清chemerin的独立影响因素。结论血清omentin-1可以反映孕妇糖、脂代谢紊乱和胰岛素抵抗程度,血清Chemerin则提示患者的高脂血症和慢性炎症状态。两者与GDM关系密切,可能共同参与了GDM疾病的发生和发展。  相似文献   
5.
Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.Obesity and the metabolic syndrome are major risk factors for a wide array of diseases, including type 2 diabetes mellitus, cardiovascular disease, and cancer (1, 2). Compelling evidence shows that metabolic syndrome is caused, in part, by a suboptimal intrauterine environment (3). The strong association between maternal obesity during pregnancy and metabolic syndrome in childhood is of particular concern because almost two-thirds of American women now enter pregnancy either overweight or obese (4). Obesity during pregnancy therefore creates a vicious, detrimental cycle of intrauterine transmission of metabolic disease from the mother to her children (5). Intervention strategies involving lifestyle changes or antiobesity drugs remain largely unsuccessful, and it is therefore urgent to explore the possibility of intervening in utero to prevent the development of obesity and metabolic syndrome.Obesity in pregnant women is associated with activation of placental insulin and mechanistic target of rapamycin complex 1 (mTORC1) signaling, up-regulation of specific placental amino acid transporters, and fetal overgrowth (6, 7). In addition, circulating levels of adiponectin (ADN) are decreased in obese pregnant women (8, 9). The ADN protein is synthesized in adipose tissue and undergoes tightly regulated multimerization involving chaperone proteins, including disulfide-bond A oxidoreductase-like protein (DsbA-L), resulting in the assembly of oligomeric ADN proteins of different molecular weight (10). Multimerization into the high-molecular-weight (HMW) form increases the t1/2 of ADN (11), and the insulin-sensitizing effect of ADN can largely be attributed to the HMW form (12). Low circulating levels of HMW ADN strongly predict the development of gestational diabetes mellitus (GDM) independent of maternal adiposity (13, 14).We recently reported that ADN, in contrast to its well-known insulin-sensitizing effects in skeletal muscle and liver, inhibits insulin and mTORC1 signaling and amino acid transport in cultured primary human trophoblast (PHT) cells (15) and in pregnant mice in vivo (16). This effect is mediated by activation of trophoblast peroxisome proliferator-activated receptor-α (PPARα) signaling and increased ceramide synthesis, resulting in inhibition of IRS-1 (17). Thus, low circulating ADN in maternal obesity may be causally linked to changes in placental function and increased fetal growth. These findings, together with the recent discovery of an orally active ADN receptor agonist (AdipoRon) (18), provide the rationale for exploring the possibility that maternal ADN supplementation may prevent the adverse fetal outcomes in maternal obesity.We recently established a mouse model of obesity in pregnancy, which shows extensive similarities to the human condition, including low maternal ADN and glucose intolerance, increased placental nutrient transport, and fetal overgrowth (19). In this study, we used this model to test the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin signaling and nutrient transport, and prevents fetal overgrowth.  相似文献   
6.
目的观察脂肪因子Omentin-1、脂联素与中老年女性骨密度之间的相关性。方法选取2017年3月至2018年4月在佛山市中医院就诊的338名女性,按照绝经状态分为围绝经期/绝经期组(n=194)和绝经后组(n=124)。将参研人员年龄、体质量指数(bone mass index,BMI)、腰围、吸烟状况、身体活动、脂联素、Omentin-1和激素进行多变量调整(ANCOVA),用于研究其脂肪因子和骨密度(bone mineral density,BMD)之间的潜在关系。结果与绝经后女性的腰椎BMD [(0. 69±0. 08)g/cm~2]相比,围绝经期女性的腰椎BMD[(0. 89±0. 09) g/cm~2]更高;在围绝经期/绝经期组女性中,脂联素和Omentin-1均与腰椎BMD无显著相关性(P0. 05);在绝经后组女性中,脂联素与腰椎BMD无相关性(P 0. 05);而在绝经后组女性中,Omentin-1与腰椎BMD呈显著负相关(P0. 05)。结论绝经后女性的Omentin-1与腰椎BMD呈负相关。  相似文献   
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8.
A new cardiometabolic-based chronic disease (CMBCD) model is presented that provides a basis for early and sustainable, evidence-based therapeutic targeting to promote cardiometabolic health and mitigate the development and ravages of cardiovascular disease. In the first part of this JACC State-of-the-Art Review, a framework is presented for CMBCD, focusing on 3 primary drivers (genetics, environment, and behavior) and 2 metabolic drivers (adiposity and dysglycemia) with applications to 3 cardiovascular endpoints (coronary heart disease, heart failure, and atrial fibrillation). Specific mechanistic pathways are presented configuring early primary drivers with subsequent adiposity, insulin resistance, β-cell dysfunction, and metabolic syndrome, leading to cardiovascular disease. The context for building this CMBCD model is to expose actionable targets for prevention to achieve optimal cardiovascular outcomes. The tactical implementation of this CMBCD model is the subject of second part of this JACC State-of-the-Art Review.  相似文献   
9.
The concept of food addiction (FA) is a potentially important contributing factor to the development of obesity in the general population; however, little is known about the hormonal and dietary differences between obesity with and without FA. Therefore, the aim of our study was to explore potential biomarkers, including various hormones and neuropeptides, which regulate appetite and metabolism, and dietary components that could potentially differentiate obesity with and without FA. Of the 737 adults recruited from the general Newfoundland population, 58 food-addicted and non-food-addicted overweight/obese individuals (FAO, NFO) matched for age, sex, BMI and physical activity were selected. A total of 34 neuropeptides, gut hormones, pituitary polypeptide hormones and adipokines were measured in fasting serum. We found that the FAO group had lower levels of TSH, TNF-α and amylin, but higher levels of prolactin, as compared to NFO group. The total calorie intake (per kg body weight), the dietary intake of fat (per g/kg body weight, per BMI and per percentage of trunk fat) and the percent calorie intake from fat and carbohydrates (g/kg) was higher in the FAO group compared to the NFO group. The FAO subjects consumed more sugar, minerals (including sodium, potassium, calcium and selenium), fat and its components (such as saturated, monounsaturated and trans fat), omega 3 and 6, vitamin D and gamma-tocopherol compared to the NFO group. To our knowledge, this is the first study indicating possible differences in hormonal levels and micro-nutrient intakes between obese individuals classified with and without food addiction. The findings provide insights into the mechanisms by which FA could contribute to obesity.  相似文献   
10.
Limiting food intake attenuates many of the deleterious effects of aging, impacting upon healthspan and leading to an increased lifespan. Whether it is the overall restriction of calories (calorie restriction: CR) or the incidental reduction in macronutrients such as protein (protein restriction: PR) that mediate these effects is unclear. The impact of 3 month CR or PR, (10 to 40%), on C57BL/6 mice was compared to controls fed ad libitum. Reductions in circulating leptin, tumor necrosis factor-α and insulin-like growth factor-1 (IGF-1) were relative to the level of CR and individually associated with morphological changes but remained unchanged following PR. Glucose tolerance and insulin sensitivity were improved following CR but not affected by PR. There was no indication that CR had an effect on oxidative damage, however CR lowered antioxidant activity. No biomarkers of oxidative stress were altered by PR. CR significantly reduced levels of major urinary proteins suggesting lowered investment in reproduction. Results here support the idea that reduced adipokine levels, improved insulin/IGF-1 signaling and reduced reproductive investment play important roles in the beneficial effects of CR while, in the short-term, attenuation of oxidative damage is not applicable. None of the positive effects were replicated with PR.  相似文献   
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