内脏脂肪区域、体脂肪率及血脂异常与糖尿病前期的关系

目的 了解内脏脂肪区域(visceral fat area,VFA)、体脂肪率(body fat percentage,BFP)、血脂异常与糖尿病前期(impaired glucose regulation,IGR)的关系并探讨IGR的危险因素。 方法 采用病例-对照法,选择克拉玛依市中心医院健康管理中心确诊糖尿病前期组238人,血糖正常组292人进行体格测量、生化指标及人体成分检测,采用logistic回归分析糖尿病前期的危险因素。 结果 IGR组的体重指数(body mass index,BMI)、甘油三酯(triglyceride,TG)、高密度脂蛋白(high density lipoprotein,HDL)、VFA均高于血糖正常组(P<0.05),BFP与血糖正常组比较差异无统计学意义(P>0.05);IGR组中高TG血症、高TC血症及高LDL血症的检出率分别为26.50%、10.90%、8.80%,均高于血糖正常组(P<0.05);二分类logistic回归分析显示,肥胖(OR=2.035,95%CI:1.183~3.501),VFA≥111.74 cm²(OR=1.910,95%CI:1.183~3.501),高TG血症者(OR=2.779,95%CI:1.685~4.582)为糖尿病前期的危险因素。 结论 糖尿病前期与肥胖、内脏脂肪区域及高TG血症有关,未发现体脂率水平与糖尿病前期有关系。     

高尿酸血症合并糖尿病前期患者血尿酸与高敏C反应蛋白及胰岛素抵抗的关系

目的 探讨高尿酸血症合并糖尿病前期患者血尿酸(serum uric acid,SUA)水平与高敏C反应蛋白(high sensitivity C-reactive protein,hs-CRP)、胰岛素抵抗的关系.方法 168例高尿酸血症患者分为2组,112例合并糖尿病前期者为合并组,56例未合并者为未合并组;选择同期40例体检健康者为对照组.检测各组SUA、hs-CRP、空腹血糖(fasting plasma glucose,FPG)、空腹胰岛素(fasting insulin,FINS),计算胰岛素抵抗指数(homeostasis model assessment of insulin resistance,HOMA-IR),并进行组间比较.结果 合并组与未合并组hs-CRP((3.95±2.97)、(2.36±1.54)mg/L)、SUA((517.00±40.00)、(475.00±68.00)μmol/L)、FPG((6.65±0.42)、(5.61±0.51) mmol/L)、HOMA-IR (5.10±1.30、3.80±0.90)均高于对照组((0.76±0.51)mg/L、(360.00±41.00)μmol/L、(5.07±0.32) mmol/L、2.50±1.10)(P＜0.05);合并组以上指标均高于未合并组,差异有统计学意义(P＜0.05).结论 高尿酸血症合并糖尿病前期患者SUA水平与hs-CRP、HOMA IR、FPG相关.     

Associations between Dietary Patterns and Impaired Fasting Glucose in Chinese Men: A Cross-Sectional Study

Few studies have examined the association between Asian dietary pattern and prediabetes, in particular, the Chinese diet. We conducted a cross-sectional study to identify dietary patterns associated with impaired fasting glucose (IFG) which considered a state of prediabetes in Chinese men. The study included 1495 Chinese men aged 20 to 75 years. Information about diet was obtained using an 81-item food frequency questionnaire (FFQ), and 21 predefined food groups were considered in a factor analysis. Three dietary patterns were generated by factor analysis: (1) a vegetables-fruits pattern; (2) an animal offal-dessert pattern; and (3) a white rice-red meat pattern. The multivariate-adjusted odds ratio (OR) of IFG for the highest tertile of the animal offal-dessert pattern in comparison with the lowest tertile was 3.15 (95% confidence intervals (CI): 1.87–5.30). The vegetables-fruits dietary pattern was negatively associated with the risk of IFG, but a significant association was observed only in the third tertile. There was no significant association between IFG and the white rice-red meat pattern. Our findings indicated that the vegetables-fruits dietary pattern was inversely associated with IFG, whereas the animal offal-dessert pattern was associated with an increased risk of IFG in Chinese men. Further prospective studies are needed to elucidate the diet-prediabetes relationships.     

Blueberries Improve Endothelial Function,but Not Blood Pressure,in Adults with Metabolic Syndrome: A Randomized,Double-Blind,Placebo-Controlled Clinical Trial

Blueberry consumption has been shown to have various health benefits in humans. However, little is known about the effect of blueberry consumption on blood pressure, endothelial function and insulin sensitivity in humans. The present study investigated the role of blueberry consumption on modifying blood pressure in subjects with metabolic syndrome. In addition, endothelial function and insulin sensitivity (secondary measurements) were also assessed. A double-blind and placebo-controlled study was conducted in 44 adults (blueberry, n = 23; and placebo, n = 21). They were randomized to receive a blueberry or placebo smoothie twice daily for six weeks. Twenty-four-hour ambulatory blood pressure, endothelial function and insulin sensitivity were assessed pre- and post-intervention. The blood pressure and insulin sensitivity did not differ between the blueberry and placebo groups. However, the mean change in resting endothelial function, expressed as reactive hyperemia index (RHI), was improved significantly more in the group consuming the blueberries versus the placebo group (p = 0.024). Even after adjusting for confounding factors, i.e., the percent body fat and gender, the blueberry group still had a greater improvement in endothelial function when compared to their counterpart (RHI; 0.32 ± 0.13 versus −0.33 ± 0.14; p = 0.0023). In conclusion, daily dietary consumption of blueberries did not improve blood pressure, but improved (i.e., increased) endothelial function over six weeks in subjects with metabolic syndrome.     

The cation efflux transporter ZnT8 (Slc30A8) is a major autoantigen in human type 1 diabetes

Type 1 diabetes (T1D) results from progressive loss of pancreatic islet mass through autoimmunity targeted at a diverse, yet limited, series of molecules that are expressed in the pancreatic beta cell. Identification of these molecular targets provides insight into the pathogenic process, diagnostic assays, and potential therapeutic agents. Autoantigen candidates were identified from microarray expression profiling of human and rodent pancreas and islet cells and screened with radioimmunoprecipitation assays using new-onset T1D and prediabetic sera. A high-ranking candidate, the zinc transporter ZnT8 (Slc30A8), was targeted by autoantibodies in 60-80% of new-onset T1D compared with <2% of controls and <3% type 2 diabetic and in up to 30% of patients with other autoimmune disorders with a T1D association. ZnT8 antibodies (ZnTA) were found in 26% of T1D subjects classified as autoantibody-negative on the basis of existing markers [glutamate decarboxylase (GADA), protein tyrosine phosphatase IA2 (IA2A), antibodies to insulin (IAA), and islet cytoplasmic autoantibodies (ICA)]. Individuals followed from birth to T1D showed ZnT8A as early as 2 years of age and increasing levels and prevalence persisting to disease onset. ZnT8A generally emerged later than GADA and IAA in prediabetes, although not in a strict order. The combined measurement of ZnT8A, GADA, IA2A, and IAA raised autoimmunity detection rates to 98% at disease onset, a level that approaches that needed to detect prediabetes in a general pediatric population. The combination of bioinformatics and molecular engineering used here will potentially generate other diabetes autoimmunity markers and is also broadly applicable to other autoimmune disorders.     

Dissonance in the discourse of the duration of diabetes: A mixed methods study of patient perceptions and clinical practice

BackgroundRemission of diabetes can be rewarding for patients and physicians, but there is limited study of how patients perceive the timeline of a disease along the continuum of glycaemic control.ObjectiveTo explore how patients perceive the timeline of diabetes along the continuum of glycaemic control and their goals of care and to identify whether family physicians communicate the principles of regression and remission of diabetes.DesignMixed methods approach of qualitative semi‐structured interviews with purposive sampling followed by cross‐sectional survey of physicians.ParticipantsThirty‐three patients living with prediabetes (preDM) or type 2 diabetes mellitus (T2DM) at medical centres in Georgia and Nevada; and 387 family physicians providing primary care within the same health system.ResultsPatients described two timelines of diabetes: as a lifelong condition or as a condition that can be cured. Patients who perceived a lifelong condition described five treatment goals: reducing glucose‐related laboratory values, losing weight, reducing medication, preventing treatment intensification and avoiding complications. For patients who perceived diabetes as a disease with an end, the goal of care was to achieve normoglycaemia. In response to patient vignettes that described potential cases of remission and regression, 38.2% of physician respondents would still communicate that a patient has preDM and 94.6% would tell the patient that he still had diabetes.ConclusionsMost physicians here exhibited reluctance to communicate remission or regression in patient care. Yet, patients describe two different potential timelines, including a subset who expect their diabetes can be ‘cured’. Physicians should incorporate shared decision making to create a shared mental model of diabetes and its potential outcomes with patients.Patient or Public ContributionIn this mixed methods study, as patients participated in the qualitative phase of this study, we asked patients to tell us what additional questions we should ask in subsequent interviews. Data from this qualitative phase informed the design and interpretation of the quantitative phase with physician participants.     

Balancing needs and means: the dilemma of the β-cell in the modern world

The insulin resistance of type 2 diabetes mellitus (T2DM), although important for its pathophysiology, is not sufficient to establish the disease unless major deficiency of β-cell function coexists. This is demonstrated by the fact that near-physiological administration of insulin (CSII) achieved excellent blood glucose control with doses similar to those used in insulin-deficient type 1 diabetics. The normal β-cell adapts well to the demands of insulin resistance. Also in hyperglycaemic states some degree of adaptation does exist and helps limit the severity of disease. We demonstrate here that the mammalian target of rapamycin (mTOR) system might play an important role in this adaptation, because blocking mTORC1 (complex 1) by rapamycin in the nutritional diabetes model Psammomys obesus caused severe impairment of β-cell function, increased β-cell apoptosis and progression of diabetes. On the other hand, under exposure to high glucose and FFA (gluco-lipotoxicity), blocking mTORC1 in vitro reduced endoplasmic reticulum (ER) stress and β-cell death. Thus, according to the conditions of stress, mTOR may have beneficial or deleterious effects on the β-cell. β-Cell function in man can be reduced without T2DM/impaired glucose tolerance (IGT). Prospective studies have shown subjects with reduced insulin response to present, several decades later, an increased incidence of IGT/T2DM. From these and other studies we conclude that T2DM develops on the grounds of β-cells whose adaptation capacity to increased nutrient intake and/or insulin resistance is in the lower end of the normal variation. Inborn and acquired factors that limit β-cell function are diabetogenic only in a nutritional/metabolic environment that requires high functional capabilities from the β-cell.     

Immunoregulatory dysfunctions in type I diabetes: Natural and antibody-dependent cellular cytotoxic activities

Peripheral blood lymphocytes from 13 patients with established insulin-dependent diabetes mellitus (IDDM) and 2 prediabetic patients were examined for natural killer (NK) and antibody-dependent cellular cytotoxic activities (ADCC), lectin-dependent cellular cytotoxicity (LDCC), interferon- and interleukin-2-induced cytotoxicity, and concanavalin A-induced suppressor-cell activities in comparison with age-matched normal controls. IDDM patients demonstrated normal levels of NK and ADCC activities against K562 and antibody-coated SB target cells, respectively, compared to controls. IDDM patients showed normal levels of LDCC activity. Notable deviations from control values were, however, observed with diabetic lymphocytes in the following systems. Interferon-and interleukin-2-induced NK activities were significantly higher with IDDM lymphocytes than with control cells. IDDM lymphocytes precultured with concanavalin A demonstrated lower NK and ADCC activities than control cells and manifested decreased suppressor effects on the NK activity of normal allogeneic lymphocytes. Lymphocytes from one of two prediabetic patients showed increased NK, ADCC, and LDCC activities in comparison to controls. The increased interferon- and interleukin-2-induced enhancement of NK activity and reduced suppressor activity of lymphocytes from IDDM patients may be involved in the pathogenesis of the disease.     

Effect of vitamin D supplementation on glycose homeostasis and islet function in vitamin D deficient or insufficient diabetes and prediabetes: a systematic review and meta-analysis

Objective of the present study was to evaluate the effect of vitamin D supplementation on glycose homeostasis, islet function, and diabetes progress. Literatures were searched via electronic databases, websites, and previous reviews from the earliest available time to the end of May 2020. Randomized controlled trials initially designed for diabetes and prediabetes with 25-dihydroxyvitamin D [25(OH)D]<30 ng/ml were included. All data were analyzed and presented based on the Cochrane guidelines and PRISMA guidelines. In total, 27 articles (n = 1,932) were enrolled in this study. Vitamin D supplementation significantly improved fasting blood glucose, postprandial blood glucose, and quantitative insulin sensitivity check index in diabetes and prediabetes with baseline 25(OH)D<30 ng/ml. Higher percentages regressing from prediabetes to normal glucose status [1.60 (1.19, 2.17), p = 0.002, n = 564] and lower percentage progressing from prediabetes to diabetes [0.68 (0.36, 1.27), p = 0.23, n = 569] were found in the supplementation group. The positive effects of vitamin D supplementation on body mass index, waist, HDL-C, LDL-C, and CRP were also demonstrated. In conclusion, modest improvements in vitamin D supplementation on short-term glycose homeostasis, insulin sensitivity, and disease development in diabetes and prediabetes with 25(OH)D<30 ng/ml were demonstrated, but more research needs to be conducted in the future to support the clinical application. (Register ID: CRD42020186004)