Volume 02 · Issue 05 · 2010

At a 2008 forum entitled "Combating the Global Obesity Epidemic: Small Moves or Big Changes?", experts pointed out that more than 1 billion adults worldwide are currently overweight, while at least 300 million people are clinically obese. Medical experts call this global obesity epidemic "global obesity". Obesity is now spreading like a plague around the world, and the World Health Organization predicts that by 2015, there will be 2.3 billion overweight adults and 700 million obese patients.

To observe the effectiveness of creatine phosphate (CP) in the elderly diabetic patients combined with heart failure (HF).

Sixty elderly diabetic patients combined with HF (NYHA Ⅲ to Ⅳ grade) were enrolled in Sichuan Provincial People’s Hospital from February to June in 2009, and adopting sortition was randomly assigned to the control group (n=30) and the treatment group (n=30). In keeping glucose, blood pressure and lipid to reach purpose, subjects of the control group received routine treatment, including general treatment and medication such as diuretic, angiotensin converting enzyme inhibitor or angiotensinⅡ receptor blocker, beta-receptor blocker, positive inotropic, and aldosterone receptor antagonist. Those of the treatment group additionally had 2.0 g CP once per day. Glucose, insulin, C-peptide, glycosylated hemoglobin, plasma brain natriuretic peptide (BNP), AMP-activated protein kinase (AMPK) were tested before and after the intervention. t test was used for data analysis.

After the intervention, 6-minute walking test (6MWT), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS) and E peak and A peak ratio (E/A ratio) were significantly improved in both groups (t values were 2.776 and 3.099, both P<0.05). After the intervention, BNP, AMPK, insulin resistance (IR) and insulin sensitivity index were significantly improved in both groups. AMPK ((12±4) vs (10±5) ng/L) and IR (1.7±0.9 vs 0.9±0.4) were found to be significantly different between the treatment group and the control group (t values were 2.586 and 4.258, both P<0.05).

CP may be able to significantly improve myocardium energy metabolism, correct insulin resistance and regulate myocardial relaxation function, so as to improv clinical symptom and prognosis of elderly diabetic patients combined with HF.

To compare the clinical features of fulminant type 1 diabetes mellitus with classic type 1 diabetes mellitus and to explore the mechanism of fulminant type 1 diabetes mellitus.

Of the patients admitted in our hospital from September 2005 to September 2009, six were diagnosed with fulminant type 1 diabetes (F group) and 24 were diagnosed with classic type 1 diabetes (NF group). Their medical data, including flu-like symptoms, nausea, vomiting or abdominal pain, blood glucose, HbA1c, C peptide, alanine aminotransferase, creatine kinase, creatinine, blood potassium, and blood white cell count were retrospectively analyzed.χ² or t test was used for data analysis.

In comparison with the NF group, the age of onset of F group was higher ((46±6)vs (19±6)years, t=9.89, P<0.01), the course of disease was shorter ((3.5±2.7) vs (52.5±32.6) d, t=3.63, P<0.01), flu-like symptoms were more commonly seen (50%(3/6) vs 0 (0/24), χ²=13.33, P<0.01), nausea, vomiting or abdominal pain were also increased (83%(5/6) vs 0(0/24), χ²=24.00, P<0.01). The blood glucose of the F group was higher than that of the NF group ((44±7) vs (23±4) mmol/L, t=9.22, P<0.01), HbA1c was decreased ((7.1±1.0)% vs (14.4±2.2)%, t=7.66, P<0.01), 2-h C peptide was lower ((0.21±0.17) vs (0.58±0.39) μg/L, t=2.29, P<0.05), alanine aminotransferase was higher ((206±124) vs (10±2) U/L, t=8.18, P<0.01), the creatine kinase was increased ((1038±447)vs (79±10) U/L, t=11.11, P<0.01), creatinine was also increase ((179±39)vs (55±16) μmol/L, t=12.33, P<0.01), blood kalium was higher ((5.2±0.7) vs (3.4±0.8) mmol/L, t=5.07, P<0.01), the blood white cell count was more ((21.0±8.1)×10⁹/L vs (6.0±1.9)×10⁹/L, t=8.64, P<0.01).

Islet beta-cell function failure, serious metabolic disorder, more intense immune response and multiple organ dysfunctions may be found in patients with fulminant type 1 diabetes mellitus.

To explore the effect of SOX13 antibody(sry related HMG box 13-antibody, SOX13-Ab)on islet β cell function and to further determine the characteristics of autoimmune response of SOX13-Ab in ketosis-prone diabetes(KPD).

During the period from January 2005 to November 2009, the 245 KPD patients (male: 138, female: 107; age: 33(1.0 to 80.0)years) who visited a doctor in Department of Endocrinology at Nanjing Drum Tower Hospital were recruited and screened for SOX13-Ab, GDA-Ab and IA-2A. Then according to SOX13-Ab, GAD-Ab and IA-2A status, the diabetes were divided into SOX13-Ab, GAD-Ab, IA-2A positive groups and antibody-negative group. The effect of SOX13-Ab on islet β cell function was evaluated by comparison of C-peptide levels among the four subgroups. The mean levels of C-peptide in different subgroups were expressed as median(IQR), then analysed with ANOVA after being ln-transformed.

The fasting C-peptide(FCP)and/or postprandial C-peptide(PCP)levels in SOX13-Ab or GAD-Ab positive groups were significantly lower than that in antibody-negative group among female KPD (FCP: 166.0(300.0)vs 287.5(302.7)pmol/L, 166.5(159.3)vs 287.5(302.7)pmol/L; PCP: 285.0(527.0)vs 528.0(774.0)pmol/L, 231.0(502.5)vs 528.0(774.0)pmol/L, all P<0.05) or KPD patients with age-onset ≤40 years (FCP: 166.0(56.0)vs 228.0(250.0)pmol/L, 166.0(241.8)vs 228.0(250.0)pmol/L, all P<0.05) or duration ≤ 5 years (FCP: 191.0(137.5)vs 324.0(340.0)pmol/L, 167.1(223.1) vs 324.0 (340.0)pmol/L, all P<0.05). While among patients with duration>5 years, the levels of FCP in GAD-Ab positive group were significantly lower than that in SOX13-Ab positive group (130.0(458.8)vs 189.5(357.7)pmol/L, P<0.05). The comparison of β cell function among groups with different islet antibody status was made using an ANOVA model, which showed that no significant difference in FCP and PCP levels between SOX13-Ab positive and antibody-negative group, while the difference in FCP levels was significant between GAD-Ab/SOX13-Ab positive and antibody-negative group. There was significantly adverse relationship between duration and β cell function in KPD patients positive for GAD-Ab or IA-2A(GAD-Ab: r=-0.500, P=0.007; IA-2A: r=-0.821, P=0.023), while in KPD patients positive for SOX13-Ab, there was no significantly adverse relationship between duration and β cell function(r=-0.104, P=0.606).

The effect of SOX13-Ab is less marked than that of GAD-Ab on β cell function in KPD patients.

To study the meaning of serum retinal binding protein 4 in type 2 diabetes with diabetic retinopathy.

Serum RBP4 and transthyretin (TTR) of 35 patients with diabetic retinopathy (DR) were crosssectionally measured by enzyme linked immunosorbent assay (ELISA). Thirty-seven diabetic patients without diabetic retinopathy (NDR) and 30 nondiabetic subjects (NGR) were enrolled as controls. In each subject, fasting values of glucose, insulin, total cholesterol(TC), triglyceride (TG), low density lipoprotein(LDL), high density lipoprotein(HDL), C-reactive protein (CRP), and HbA1c were determined.

Serum RBP4 level in patients with DR was significantly higher than that in NGR((15±4) mg/L, (13±3) mg/L, t=3.74, P<0.05), but there was no difference between patients with and without DR ((15±4) mg/L, (15±3) mg/L, t=1.73, P=0.073). However, the RBP4/ TTR ratio in patients with DR was markedly increased than that NDR and NGR (0.12±0.06, 0.09±0.04 and 0.072±0.021, F=9.562, both P<0.05). In addition, RBP4 and the RBP4/TTR ratio were analyzed respectively according to Binary Logistic Backward·RBP4(B=0.214, OR=1.239, P<0.05)and RBP4/TTR ratio(B=0.718, OR=2.051, P<0.05)were found to be the risk factors for diabetic retinopathy, and the RBP4/TTR ratio was more contributive than serum RBP4 concentration in type 2 diabetes companied with diabetic retinopathy.

The RBP4/TTR ratio is more valuable than serum RBP4 concentration to evaluate risk factor of diabetic retinopathy, and RBP4 may be a novel causative agent for diabetic retinopathy of type 2 diabetes mellitus.

To investigate the relationship between small ubiquitin-like modifer 4 M55V polymorphism with type 2 diabetes and related factors.

We analyzed the SUMO4 M55V polymorphism of 427 newly diagnosed type 2 diabetic patients, who were diagnosed firstly at outpatient and inpatient in Zhongnan Hospital of Wuhan University from 2006 February to 2009 September, with 281 healthy controls, by PCR-RFLP assay, and gathered their body height, weight, waistline, blood pressure on an empty stomach. Blood glucose, insulin and HbA1c also measured. Then analyzed the relationship between SUMO4 M55V polymorphism with type 2 diabetes and its related factors, with using logistic analysis for evaluating the risk factors of type 2 diabetes.

Compared with the control group, the levels of waist circumference(t=2.72, P<0.01), BMI(t=2.66, P<0.01), FBG(t=2.81, P<0.01), PPBG(t=3.07, P<0.01)HbA1c(t=2.79, P<0.01) and TG(t=2.63, P<0.01) are significantly higher in T2DM group(P<0.01). The frequency of GG genotype was significantly higher in T2DM group(compare with the three genotypes: χ²=6.782, P<0.05), and the risk of type 2 diabetes is two times higher in GG genotype compared with AA genotype (OR=2.011). Logistic multifactor analysis found that there is notable association between type 2 diabetes incidence with HbA1c(P<0.05, OR=2.57, 95%CI: 1.92-4.63), body weight(P<0.05, OR=2.61, 95%CI: 1.74-4.37), SUMO4 M55V polymorphism (P<0.05, OR=1.47, 95%CI: 1.09-3.42), TG(P<0.05, OR=1.59, 95%CI: 1.24-4.63). Further analysis of HbA1c, BMI, TG, FINS and HOMA-IR showed that there was significant difference of TG among different genotypes(F=3.382, P<0.05), and compared with AA genotype, levels of FINS(F=4.075, P<0.05) and HOMA-IR(F=14.389, P<0.001) in AG and GG were also higher.

SUMO4 M55V polymorphism is associated with the incidence of type 2 diabetes among the Han population in Hubei.

To investigate the correlation between catch-up fat following food restriction and plasma glucose-dependent insulinotropic polypeptide (GIP) concentration in rats.

Sixty Sprague-Dawley rats were randomly divided into the normal control group (NC group, n=15), refed with normal diet group (RN group, n=15), high fat diet group (HF group, n=15) and refed with high fat diet group (RH group, n=15). The body weight and food intake of rats were recorded. Animals were sacrificed at 4, 6, 8 weeks respectively before determination of body fat and plasma GIP concentration. Differences between the groups were evaluated using paired t-test with SPSS 13.0 statistical software, and differences between the groups at the same time point were evaluated using one-way ANOVA. The one-way line correlation analysis was used to assess the correlation of catch-up fat and plasma GIP concentration.

Compared with the control group, both body fat content ((3.6±0.6), (7.9±1.5), (4.6±1.1), and (7.0±1.0) g; t values were-2.601, -2.305, and-2.501; all P<0.05) and GIP concentration ((41±9), (61±7), (51±8), and (59±8) pmol/L; t values were-6.061, -3.452, and-4.651; all P<0.05) were increased in the HF group, RN group and RH group. Statistical analysis showed a close correlation between body fat content and GIP concentration(r²=0.9407).

There is a close correlation between catch-up fat and plasma GIP concentration, which may result from pathophysiological changes caused by catch-up growth.

To study the roles of aldose reductase in the development of diabetic nephropathy using mouse models which were deficient for aldose reductase (AR).

Eight-week-old homozygous male AR-knockout (KO), bitransgenic (BT) and wild-type (WT) background C57BL/6 mice were treated with or without 40 μg/g streptozotocin by intraperitoneal injection. After 2 weeks, blood glucose was measured and hyperglycemia was confirmed. Diabetic and control mice were further maintained for 17 weeks, then sacrificed. Body weight, kidney weight, serum glucose, triglyceride, cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, blood urea nitrogen, serum creatinine, glomerular filtration rate and urinary albumin parameters were determined. PAS staining was performed for kidney histological analyses. Western blot and immunohistochemistry were used to determine the expression of collagen Ⅳ and transforming growth factor-beta1 (TGF-β₁). Protein kinase C (PKC) activities for the cytoplasm and cell membrane fractions of the renal cortex were assayed with the kit of PepTag^® Assay for non-radioactive detection of PKC. One-way ANOVA was used for multiple comparisons.

In comparison with the diabetic mice with normal aldose reductase activity, most serum and urinary parameters as well as renal histological and functional parameters were significantly improved in diabetic mice deficient in aldose reductase. For instance, loss of AR in the KO mice results in 43% reduction in urine albumin ((1.49±0.26) vs (2.62±0.34)mg/g creatinine, F=20.8, P<0.01) whereas a 48% reduction was resulted in the BT mice ((1.36±0.12) vs (2.62±0.34) mg/g creatinine, F=20.8, P<0.01). Further, aldose reductase deficiency prevented hyperglycemia-induced activation of PKC and TGF-β₁.

AR contributes to the development of diabetic nephropathy in vivo. The inhibition of AR may be beneficial for the prevention and treatment of the disease.

To investigate whether the advanced glycation end products (AGEs) can induce the apoptosis of rat retinal microvascular endothelial cells and the related mechanisms.

Twenty SPF male Wistar rats aged 7 to 8 weeks were used. Microvascular endothelial cells was isolated from rat retinal, and identified by immunofluorescence staining and flow cytometry for vWF, and the tube formation on Matrigel. MTT assay was used to analyze the effect of AGEs on the proliferation of rat retinal microvascular endothelial cells. Flow cytometry was used to detect AGEs-induced apoptosis. Reverse transcription PCR and flow cytometry were used to analyze the expression level of RAGE, PKC, ICAM-1 and iNOS with or without AGEs in culture medium. t-test were used for statistical analysis.

The isolated and purified rat retinal microvascular endothelial cells express vWF, and can form capillary-like network structure in Matrigel. AGEs can inhibit proliferation of rat retinal endothelial cells in dose- and time-dependent ways: the proliferation of endothelial cells in 200 mg/L AGEs group was lower than control at 5-day(t=8.9, P<0.05), and more significant at 7- and 9-day (t=15.7 or 46.1, both P<0.01). The inhibition to proliferation of endothelial cells by 400 mg/L AGEs was significant at 3-day(t=12.5, P<0.05), and became greatly at 5-, 7- and 9-day(t=22.4, 41.5 or 77.7, all P<0.01). AGEs also induced apoptosis of retinal endothelial cells. Furthermore, AGEs can up-regulate the expression of RAGE, PKC, iNOS and ICAM-1 at mRNA level(t=91.8, 9.22, 16 and 42, both P<0.01) and protein level(t=20.2, 12.3, 7.7 and 13.9, all P<0.01).

AGEs might induced phenotypic and functional changes of rat retinal microvascular endothelial cells by up-regulating RAGE.

To observe the effects of glucose on the expression of alkaline phosphatase(ALP), bone morphogenetic protein-2(BMP-2) and transforming growth factor-beta l (TGF-β₁) for rat bone marrow stromal cells (BMSCs) differentiation into osteoblastic(OB) and to investigate the mechanism of the impact on the bone metabolism from them.

Bone-marrow stromal cells were achieved from long bone marrow of rats under aseptic condition. After purification, passage and amplification by using the whole bone marrow adherence method, the BMSCs were interfered into osteoblasts with different doses of glucose concentration (5.5 mmol/L and 25.0 mmol/L) in the presence of the osteogenic medium. The rate of mineralization was examined by staining of mineralized nodules with Alizarin red S, and the difference of ALP, BMP-2 and TGF-β₁ between interblocks was examined by enzyme linked immunosorbent assay (ELISA) after 21 d of culture. One way analysis of variance was used for statistical analysis between groups.

Compared with 5.5 mmol/L glucose classic group, the rate of mineralization was cut down significantly in 25.0 mmol/L glucose classic group ((45.3±0.7)% vs(68.3±0.8)%, P<0.05), and the activity of ALP(0.350±0.020, 0.563±0.043), BMP-2 ((590±27), (744±41)μg/L) and TGF-β₁ ((875±40), (1188±52)μg/L)were also cut down significantly (all P<0.05).

High concentration glucose inhibits the differentiation of BMSCs into osteoblastics, which provids a potential mechanisms of diabetes-induced osteoporosis.

As a chronic and frequently occurring disease that seriously affects human health, type 2 diabetes has become a health and social problem of common concern around the world, and its pathogenesis is a hot spot of research at present. Recently, more and more researchers have paid attention to the correlation between uncoupling protein 2 (UCP2) and type 2 diabetes, and found that UCP2 participates in and affects multiple links in the occurrence and development of type 2 diabetes. It can be seen that in-depth research on the role of UCP2 will help to enrich the theory of diabetes pathogenesis and explore new targets for diabetes treatment. This article will review the latest research results of UCP2 and type 2 diabetes.

With the change of lifestyle and eating habits, obesity and overweight people are increasing rapidly, which has become an important social and public health problem, and is listed as one of the top ten risk factors leading to disease burden by the World Health Organization. Obesity is not only a high risk factor for diabetes, cardiovascular and cerebrovascular diseases, hypertension and hyperlipidemia, but also can cause kidney damage. Diabetic nephropathy is a serious chronic microvascular complication of diabetes, and it is also one of the main factors that affect the quality of life and fatality of patients. Its pathogenesis includes various metabolic abnormalities, such as enhanced polyol pathway and its activity, increased advanced glycation end products (AGEs), and enhanced protein kinase C (PKC) activity. Studies have proved that obesity, especially abdominal obesity, can promote the occurrence and development of diabetic nephropathy through various metabolic pathways in the pathogenesis of diabetic nephropathy, which is one of the independent risk factors of diabetic nephropathy^[1,2]。

With the change of eating habits and lifestyle, the incidence of diabetes is on the rise worldwide, and diabetes has become a global public health problem in the 21st century. All kinds of complications caused by diabetes seriously endanger human health and bring heavy social and economic burden to countries all over the world^[1,2]。 Diabetic nephropathy is one of the most serious microvascular complications of diabetes and the leading cause of end-stage kidney disease in western countries. Statistics from the American Diabetes Society show that in the United States, diabetic nephropathy has accounted for 44.2% of the various causes of end-stage kidney disease; Chronic renal failure caused by diabetes accounted for 44% of the new patients with renal failure in 2002. It can be seen that in-depth research on the pathogenesis of diabetic nephropathy and the establishment of new treatment measures and prevention strategies on this basis will have a significant impact on public medical and health undertakings in various countries.

Adipose tissue is not only the largest energy storage organ in the body, but also acts as an endocrine organ to produce a variety of adipokines, which participate in important physiological and pathological processes, including appetite, blood pressure, reproduction, angiogenesis, insulin sensitivity, inflammation and many other links. Obesity and lipoatrophy are two kinds of metabolic diseases related to fat differentiation. One of them has too much fat and the other is too little fat, but both have insulin resistance. It can be seen that normal fat differentiation is necessary for the body to maintain the balance of energy metabolism, and abnormal fat differentiation will affect the balance of energy metabolism and even lead to diabetes.

A 58-year-old male was admitted to the hospital on 1 July 2008 due to "weakness of both lower limbs for half a year". The patient had weakness in both lower limbs in January 2008, which was obvious at the proximal end of the right lower limb and progressively aggravated. Difficulty going up and down stairs at admission, ability to walk independently on flat ground, accompanied by thigh muscle beating and deep pain, no numbness, no emaciation, no obvious weakness in both upper limbs. On a routine physical examination in 2001, the fasting blood glucose concentration was found to be about 7.0 mmol/L, and the blood glucose level was not measured at 2 h postprandial. Since then, I have not come to the hospital for diagnosis and treatment in the next 7 years. I bought Xiaoke Pill by myself and took it intermittently. My blood sugar control is unknown.

The morbidity and mortality of diabetic patients with heart failure are 4-8 times higher than those of non-diabetic patients^[1]。 It is very common for elderly diabetic patients to be hospitalized with heart failure, which is a clinical critical condition that needs to be dealt with. It not only increases clinical medical expenses, but also is an important cause of death in elderly diabetic patients, which needs further research and discussion.

In order to study the pattern of gestational diabetes, the researchers investigated 65,132 women who had two pregnancies and had given birth and 13,096 women who had three pregnancies and had given birth from 1991 to 2008 at Kaiser Hospital in Southern California, USA. This retrospective cohort study equipped each participant with a perinatal service system and physician communication records. The perinatal service system records the maternal examination pictures, behavioral characteristics and fetal and newborn conditions; The physician communication records included participants' behavioral factors, medical and childbirth processes, and complications.

Studies have reported differences in the correlation between blood glucose levels and glycosylated hemoglobin among people with impaired glucose tolerance and diabetic patients of different ethnicities. As a result, Danish researchers conducted a population study aimed at exploring whether ethnic factors influence the correlation between blood sugar and glycated hemoglobin.

The association between diabetes and cancer is unclear, and insulin resistance and secondary hyperinsulinemia are the main links in the association between diabetes and cancer.

Discovering the presence or absence of atherosclerosis in patients with type 1 diabetes is a prerequisite for reducing the risk of intervention. To this end, this study investigated the factors influencing the risk of cardiovascular disease in patients with type 1 diabetes of different genders and ages.

It has been reported that the use of exenatide (glucagon-like polypeptide-1 receptor agonist) and sitagliptin (dipeptidyl peptidase receptor blocker) may increase the risk of acute pancreatitis in patients. To this end, the researchers conducted a large retrospective cohort study to compare the risk of acute pancreatitis among diabetics, non-diabetics, and those taking exenatide, sitagliptin, and control hypoglycemic drugs.

Lifestyle improvement (especially a proper diet) is a widely recognized treatment for type 2 diabetes. Reasonable intake of energy and nutrition can not only improve dyslipidemia in diabetic patients, but also reduce the risk of complications. This randomized controlled trial was designed to evaluate the effects of enhanced dietary intervention on lipid control and risk of cardiovascular disease in patients with type 2 diabetes.

At present, there is no relevant study to explore the function and morphology of residual pancreatic islets in patients with long course of diabetes.

At present, pancreatic tissue transplantation is the only way to cure type 1 diabetes. It is of great significance to elucidate whether striated muscle can be used as a potential site for islet cell transplantation.

To date, a total of 25 gene loci significantly associated with the onset of type 2 diabetes have been identified, most of which have been identified by genomic analysis. This study performed a large-scale meta-analysis of existing genetic data aimed at discovering more type 2 diabetes susceptibility gene loci.

Previous studies have shown that continuous ambulatory blood glucose monitoring can improve the blood glucose status of adult type 1 diabetic patients with glycosylated hemoglobin ≥7.0% at enrollment; Glycated hemoglobin at enrollment<In 7.0% of patients, continuous ambulatory blood glucose monitoring can better maintain glycated hemoglobin up to standard and reduce the incidence of hypoglycemia. This study evaluated the impact of continuous ambulatory blood glucose monitoring on the quality of life of patients.

At present, the global prevalence of diabetes is increasing, with type 2 diabetes accounting for the majority. It is estimated that by 2030, the number of patients with type 2 diabetes will reach 366 million worldwide^[1]。 The increasing prevalence of obesity is one of the main reasons for the increase in the prevalence of type 2 diabetes. In 2005, about 1.4 billion adults were overweight, of which at least 400 million were obese; The above figures are expected to rise to 2.3 billion and 700 million, respectively, by 2015^[2]。 In 2002, the China Nutrition and Health Survey showed that 14.7% of Chinese people were overweight (BMI ≥25 kg/m²), and another 2.6% of Chinese people belong to the obese population (body mass index ≥30 kg/m²)^[3]。 As is the global trend, the prevalence of obesity is increasing in China. Recent studies have found that the prevalence of type 2 diabetes in the Chinese population is as high as 9.7%, and the prevalence of type 2 diabetes increases with the increase of body weight, and the body mass index<18.5, 18.5 to 24.9, 25.0 to 29.9 and ≥30 kg/m²The prevalence of type 2 diabetes mellitus was 4.5%, 7.6%, 12.8% and 18.5%, respectively^[4]。 In addition to type 2 diabetes, obesity can cause multiple organ complications throughout the body, such as hypertension, stroke and coronary atherosclerotic heart disease (hereinafter referred to as coronary heart disease). It can be seen that weight control is one of the important means to effectively prevent and treat type 2 diabetes. This article will briefly describe the harm of overweight and obesity, their relationship with type 2 diabetes and the effect of insulin therapy on body weight.