Volume 02 · Issue 02 · 2010

To investigate the outcome and risk factors of subjects with impaired glucose regulation (IGR).

A total of 192 IGR subjects from a cross-sectional survey in June to August 2002 were followed up for 5 years. Anthropometric measurement and 75 g oral glucose tolerance test were performed. The prevalence of isolated impaired fasting glucose (I-IFG), isolated impaired glucose tolerance (I-IGT), IFG+ IGT, normal glucose tolerance (NGT) and diabetes mellitus (DM) was compared. t test, Chi-square test, and analysis of variance were used for data analysis.

Five participants died during 5 years’ follow up. Of the rest 187 subjects, 79 were found to develop DM. The annual incidence of DM and NGT was 8.4 % (79/187/5-y)and 6.3%(59/187/5-y), respectively. The annual incidence of DM was 8.2 %(47/114/5-y), 6.3%(12/38/5-y) and 11.4%(20/35/5-y) for the subjects with I-IGT, I-IFG and IFG+ IGT, respectively. The risk of DM was significantly higher in IFG+ IGT subjects than I-IFT subjects. Compared with IGR subjects, those with new DM were characterized with hypertension, obesity, older age, and higher level of body mass index (BMI), waist circumference, waist-to-hip ratio and 2 h postprandial plasma glucose at baseline. BMI and systolic blood pressure during follow up were significantly higher than at baseline in subjects with new DM.

There might be a different course of I-IFG, I-IGT and IFG+ IGT progressing to DM among community residents, and there is a higher conversion rate in IFG+ IGT subjects. Various metabolic abnormalities can promote IGR progressing to DM.

To explore the association of adiponectin level, adiponectin gene-11377 polymorphism and urinary albumin excretion rate (UAER) in patients with type 2 diabetes mellitus.

Adiponectin gene SNP-11377C→G was identified in 403 patients with type 2 diabetes mellitus, including 201 patients with normal albuminuria (NAU group, UAER<30 mg/24 h), 134 patients with microalbuminuria (MiAU group, 30 mg/24 h≤UAER<300 mg/24 h) and 68 patients with macrolalbuminuria (MaAU group, UAER≥300 mg/24 h) by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Plasma adiponectin, blood lipid, fasting plasma glucose, fasting insulin serum creatinine and creatinine clearance rate were also measured.

Plasma adiponectin levels showed an increasing tendency in groups of NAU, MiAU and MaAU (6.33 mg/L(0.10-24.32), 6.97 mg/L (0.25-20.12), 9.38 mg/L(1.88-26.99)). Plasma adiponectin level was significant higher in MaAU group than in NAU and MiAU groups (P<0.01). Plasma adiponectin level was positive correlated with Scr (r=0.212, P<0.01), negative correlated with Ccr (r=-0.157, P<0.05) and HOMA-IR (r=-0.215, P<0.01). The frequencies of adiponectin gene genotype and allele showed no significant difference between the NAU group and the AU group(P>0.05). Significant difference in groups of different genotypes of SNP-11377C→G(CC/CG/GG)was not found.

Aggravation of diabetic nephropathy and albuminuria accompany increasing adiponectin level in patients with type 2 diabetes mellitus. There is no significant association of SNP-11377C→G in the promoter region of adiponectin gene and albuminuria in patients with type 2 diabetes mellitus of in a population Fujian Province.

To explore the effects of synaptopodin and WT-1 expression on the progression of diabetic nephropathy.

Thirty-five renal specimens of patients with confirmed diabetic nephropathy from January 1998 to September 2005 were selected and divided into the diffuse mesangial sclerosis group (n=20)or the nodular sclerosis group(n=15). Para-carcinoma tissues of 7 patients with renal carcinoma were regarded as controls. The expressions of synaptopodin and WT-1 in renal tissues of patients with diabetic nephropathy were detected by indirect immunofluorescence double-staining and confocal laser scanning microscope, which were analyzed by one-way ANOVA and q test. Clinical data of patients before renal biopsy were collected, including total urine protein for 24 hours (TUPr), serum creatinine (Scr) and evaluated glomerular filtration rate (eGFR), followed by analyzing with t test. Correlations between immunopathological and clinical indexes were analyzed by linear correlation.

Compared with the diffuse mesangial sclerosis group, TUPr and SCr levels were elevated (TUPr: (3.7±0.9) or (5.6±1.6) g/24 h, t=4.177, P<0.05; SCr: (92±20) or (135±45) μmol/L,t=10.455, P<0.05), and eGFR was decreased in the nodular sclerosis group ((65±19) or (53±24) ml/min,t=8.921, P<0.05). Compared with the normal controls, the number of podocytes (F=4.06, P<0.05), the expressions of synaptopodin (F=3.79, P<0.05) and WT-1 (F=5.68, P<0.05) in patients with diabetic nephropathy were significantly decreased, which were more severe in the nodular sclerotic group than in the diffuse mesangial sclerotic group (q values were 5.80, 6.42, and 5.35, respectively; all P<0.05). In diabetic nephropathy, the expressions of synaptopodin and WT-1 had a negative correlation with TUPr (r=-0.64 and -0.71, respectively; both P<0.05), and a positive correlation with eGFR (r=0.57 and 0.62, respectively; both P<0.05).

The expressions of synaptopodin and WT-1 are decreased in gelomeruli of patients with diabetic nephropathy, which correlated with clinical indexes of renal impairment. Those findings suggest that podocyte injury may be involved in the progression of diabetic nephropathy.

To investigate the relationship between leptin receptor gene Gln223Arg polymorphism and level of serum leptin and insulin resistance in subjects with normal (NGR) or impaired glucose tolerance (IGT).

Outpatients who received oral glucose tolerance test (OGTT) in our laboratory from January 2007 to August 2009 were screened. A total of 649 first-visit outpatients with normal renal and liver function and without anti-diabetic therapy were included and assigned to the NGR (n=298, 168 males and 130 females, mean age 42 years) and IGT (n=351, 188 males and 163 females, mean age 46 years) groups. Triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), HbA1c, fasting blood glucose (FBG), insulin (INS), leptin and Gln223Arg polymorphism were tested. Insulin resistance was indicated by HOMA-IR. t and χ ² tests were used for data analysis.

The IGT group showed a higher proportion of Gln223Gln genotype than the NGR group (χ²=7.38, P<0.05). TG, TC, LDL-C, FBG, HbA1c, INS, leptin and HOMA-IR were higher in the IGT group than the NGR group (t values were 13.168, 10.816, 6.704, 16.459, 26.553, 9.521, 17.108, 28.122, 5.829 and 6.602, respectively; all P<0.01). In the IGT group, subjects without the 223Arg allele showed higher TC, LDL-C, INS, leptin and HOMA-IR in comparison with carriers of the 223Arg allele (t values were 2.294, 3.744, 3.892, 7.633, 2.263 and 2.479, respectively; all P<0.05). However, no difference was found in TG, HDL-C, HbA1c and FBG (t values were 0.343, -0.494, -1.175 and 1.404, respectively; all P>0.05). Lacking 223Arg allele was associated with IGT in males (odds ratio (OR)=2.32, P<0.01) but not in females (OR=1.45, P>0.05).

The leptin receptor gene Gln223Arg polymorphism may be associated with serum lipid and leptin and insulin resistance. Males without the 223Arg allele could have higher risk of IGT.

To investigate the effects of intermittent and constant high blood glucose on the expressions of adiponectin and resistin in cultured 3T3-L1 adipocytes, nitrotyrosine formation and 8-hydroxydeoxyguanosine (8-OHdG), either in the presence or in the absence of MnTBAP or TTFA.

In vitro cultured 3T3-L1 preadipocytes were used for the intermittent high blood glucose or oxidative model. The cultured cells were then divided into two groups: group A to study changes of adiponectin and resistin mRNA and protein expression, nitrotyrosine and 8-OHdG level after intermittent or continuing exposure to 25 mmol/L glucose, MnTBAP or TTFA; group B to test adiponectin and resistin mRNA expression when intermittently or constantly exposed to H₂O₂. The adiponectin and resistin mRNA and protein expression was determined by reverse transcript polymerase chain reaction (RT-PCR) and ELISA, respectively. The production of nitrotyrosine and 8-OHdG as the oxidative stress parameter were measured.Student′s t test or analysis of variance was used for data analysis.

Compared to constant high blood glucose group, the adiponectin proteins concentration and mRNA expression level of the intermittent high blood glucose group were lower(t=7.29 or 7.13, both P<0.01), while resistin protein concentration and mRNA expression level(t=6.85 or 6.94, both P<0.01), nitrotyrosine and 8-OHdG(t=4.74 or 6.93, both P<0.01) were higher. On the other hand, the antioxidants MnTBAP and TTFA could reverse high-glucose-induced dysregulation of adiponectin(t=7.47, P<0.01) and resistin(t=6.91, P<0.01), as well as overproduction of nitrotyrosine and 8-OhdG(t=4.87 or 6.90, both P<0.01). Compared to constant exposure to H₂O_2, the adiponectin mRNA expression level with intermittent exposure to H₂O₂ was lower(t=7.21, P<0.01), and the resistin mRNA expression level with intermittent exposure to H₂O₂ was higher(t=6.79, P<0.01).

These findings suggest that intermittent high blood glucose significantly decrease adiponectin and augment resistin expression and secretion from adipocytes through reactive oxygen species overproduction at the mitochondria transport chain level.

To explore the effects of Visfatin on islet beta-cell proliferation, apoptosis and insulin secretion.

MIN6 cells were divided into three groups: control group, GFP group, and Visfatin transfection group, which were transfected by empty plasmid, GFP plasmid and 2, 5, or 10 mg/L Visfatin plasmid respectively and collected at 40 or 60 h after transfection. Visfatin mRNA and protein expression were detected by real time PCR and Western blot. Cell proliferation, apoptosis and cell cycle were detected by MTT or flow cytometry, and glucose-stimulated insulin release was detected by ELISA. ANOVA test was used for data analysis.

The proliferation of Visfatin transfected cells was significantly increased. Compared with the controls, proliferation rate of 2, 5, and 10 mg/L Visfatin plasmid at 40 h and 5 mg/L Visfatin plasmid at 60 h was increased by 1.60, 1.87, 1.75 and 1.51, respectively (t values were 4.98, 13.52, 11.02, and 6.14; all P<0.05). Palmitate-induced islet cell apoptosis decreased. Compared with the controls and GPF group, the apoptosis rate of Visfatin transfected cell was 42% and 48% lower (F values were 4.58 and 6.12; both P<0.05). Compare with the controls, the percentage of cells at G₀/G₁ phase was decreased and S phase increased in Visfatin transfected cells (F values were 5.25 and 6.23; both P<0.05). Compared with the controls, the basal insulin secretion was not changed. Glucose stimulated insulin release was increased in Visfatin transfected cells, although no significant difference was found (P>0.05).

Visfatin may promote islet beta-cell proliferation, inhibits cell apoptosis, and regulates the cell cycle.

To explore the influence of pancreatic stellate cells (PSCs) on the apoptosis of pancreatic islet cell line Ins-1 induced by high concentration of glucose.

A co-culture system was established, and Ins-1 apoptosis was evaluated by flow cytometry with Annexin IV/PI labeling after 24-hour treatment with and without 25 mmol/L glucose both in Ins-1 group and Ins-1+ PSCs group, respectively. Ins-1 vitality and nuclei morphological changes were observed with MTT and DAPI-staining respectively after 48-hour intervention with and without 25 mmol/L glucose.

Both in the Ins-1 groups and the co-cultured groups, apoptosis rates of high glucose groups were higher than those of the controls (7.93%±0.41%, 3.73%±0.35%; 11.73%±1.20%, 5.03%±0.41%; F=55.68, P<0.05), and optical densities (ODs) of the high glucose groups were lower than those of the controls (2.28±0.13, 2.85±0.31; 0.62±0.06, 1.29±0.19;F=97.75, P<0.05). Apoptosis rates of the controls, high glucose group and hyperosmotic group in co-cultured groups were significantly higher than those of corresponding group in Ins-1 single groups (5.03%±0.41%, 3.73%±0.35%; 11.73%±1.20%, 7.93%±0.41%; 7.60%±0.72%, 5.60%±0.40%;F=55.68, P<0.05), and ODs were significantly lower (1.29±0.19, 2.85±0.31; 0.62±0.06, 2.28±0.13; 0.65±0.07, 2.35±0.12;F=97.75, P<0.05), and the typical nuclei morphological changes of apoptosis cells were observed.

Hyperglycemia contributes to the deterioration of beta-cell line Ins-1, and increases its apoptosis rate, possibly intensified in the context of PSC involvement.

To construct an expressive RNA interference RNAi lentivirus specific to β-catenin, and to investigate the regulation of Wnt/β-catenin signaling on the proliferation aspect of mice pancreatic β cell line (Min6 cell).

Homologous recombination and cloning techniques were used to create the lentivirual plasmid which contains the RNAi cassette targeting the β-catenin gene. Then, the lentivirual plasmid was transfected with the other two packaging plasmids into 293T cells to product and amplify lentivirus. Dilution assay was used to titer the lentivirual stock.The β-catenin gene silencing effect induced by the RNAi lentivirus in Min6 cell was detected by real time-PCR and Western blot analysis. Finally, we transducted the RNAi lentivirus to inhibit the expression of β-catenin protein and to explore the effect of Wnt/β-catenin pathway on proliferation of mice pancreatic β cell, with MTT cell proliferation assay.

The RNAi lentivirus specific to β-catenin was produced with a titer of about 5.0×10 ⁸ TU/ml.The RNAi lentivirus could be infect Min6 cells efficiently in 3 days, and the inhibition effect was detected in 5 days after infection. The results of MTT assay suggested that inhibiting the β-catenin with the RNAi lentivirus could suppress the proliferation of Min6 cells obviously.

RNAi lentivirus is an important tool to inhibit the expression of target gene efficiently. The Wnt/β-catenin pathway plays an important role in the regulation of proliferation of mice pancreatic β cells.

To investigate the autoimmune injuries of diabetic myocardiopathy and the protective effects of immunosuppressive agent (cyclosporine A) on the injuries in streptozotocin-induced diabetic rats.

STZ-induced diabetic rats were assigned randomly to 6 groups which received low(1 mg·kg^-1·d^-1), middle (4 mg·kg^-1·d^-1) or high(8 mg·kg^-1·d^-1) dose of CsA from 1 week before or post modeling, respectively. One group of diabetic rats without any treatment (DM group), one group of insulin-treated diabetic rats (INS group) and one group of normal rats (CON group) were also monitored simultaneously as different sorts of control. The pathologic abnormalities of the heart were shown by HE, Masson stain or electromicroscopy. The deposition of immunoglobulins, IgG, IgM and IgA, was examined by immunohistochemistry and immunofluorescence.

At 8-week, interstitial fibrosis was clearly shown in diabetic heart which was accompanied by plenty of lymphocyte infiltrated. The electron microscope also indicated that myofilaments of myocardial cells were disruptive and mitochondria were degenerative. Shown by immunohistochemistry, the difference of integrated optical density (IOD) of immunoglobulins deposition among each group had statistic significance(IgG: F=11.110, P<0.01; IgA:F=10.502, P<0.01). No obvious IgG and IgA were deposited in the intercellular substance of heart in CON group (the IOD of IgG was 1482±818 and the IOD of IgA was 1053±647). But the deposition of IgG and IgA increased significantly in DM group (the IOD of IgG was 51 811±15 088,P<0.01 and the IOD of IgA was 51 881±18 170,P<0.01). There were no preventive effects of insulin on immunoglobulin deposition at all. In contrast, by CsA intervention, the deposition of immunoglobulins was diminished obviously. The outcome of immunofluorescence also demonstrated that there were statistic difference of the immunoglobulin deposition among each group (IgG: χ²=42.158, P<0.01, IgA: χ²=36.122, P<0.01, IgM: χ²=23.269, P<0.01).

The data suggest that the autoimmune injuries maybe play an important role in the pathogenesis of the diabetic myocardiopathy. Immunosuppressive treatment with CsA showed protective effects by inhibiting the immunoglobulins deposition on the diabetic myocardium.

To investigate the effects of continuous positive airway pressure(CPAP) treatment on glucose metabolism and glucocorticoid in patients with obstructive sleep apnea-hypopnea syndrome(OSAHS) and type 2 diabetes mellitus(T2DM).

To use at least 30 days of CPAP treatment on 36 cases of patients with T2DM and newly diagnosed OSAHS hospitalized during July 2008 and December 2009 in the Department of Endocrinology, Beijing Hospital. To take CPAP treatment for the patients without contraindication.Insulin sensitivity and glucose metabolism were tested and compared to the data previously obtained.Paired-t-test were used for statistical analysis.

After the application of CPAP treatment, the glycohemoglobin ((7.1±1.0)%) and fasting blood glucose((6.5±1.1) mmol/L) were lower than that been previous obtained (HbAlc(9.1±2.2)%, FBG(10.0±3.0) mmol/L; t=6.517, P<0.001;t=7.239, P<0.001), and the homeostasis model assessment (HOMA) index of insulin resistance was significantly lower compared with that obtained before the CPAP treatment (3.4±1.9 vs 2.6±2.0;t=2.204, P<0.05), but there were no significant changes of ACTH and COR(P>0.05).

CPAP can cause an overall improvement in insulin sensitivity in type 2 diabetes patients with OSAHS, CPAP is also an effective treatment in addition to lifestyle intervention and drug treatment.

The prevalence of type 2 diabetes in our population is increasing year by year, and its various metabolic disorders, complications and concomitant diseases are the main reasons leading to poor prognosis. Sleep breathing disorders are very common in patients with type 2 diabetes and often present as obstructive sleep apnea hypopnea syndrome (OSAHS). There are important clinical, epidemiological and public health links between type 2 diabetes mellitus and OSAHS. The mechanism of action and clinical treatment between type 2 diabetes mellitus and OSAHS have become one of the current research hotspots.

Numerous pathological studies have found that islet fibrosis can be observed in patients with type 1 and type 2 diabetes mellitus and in various animal models. The process of islet fibrosis further disrupts the normal tissue structure of pancreatic islets and leads to deterioration of pancreatic islet function, decrease of beta cell number and decrease of insulin secretion. Collagen type Ⅰ, collagen type Ⅲ, and fibronectin (FN) were mainly deposited in the islet fibrosis area, which was accompanied by abnormal vascular structure^[1,2]。 Therefore, islet fibrosis is an important pathological change in the process of diabetes. Islet fibrosis and transforming growth factor-beta₁(TGF-β₁) overexpression, local renin-angiotensin system (RAS) activation, oxidative stress, imbalance of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), peroxisome proliferator-activated receptor PPAR-γ, inflammatory response and macrophage infiltration. The elucidation of the mechanism of development of islet fibrosis can help to provide new therapeutic targets for the prevention and treatment of diabetes. This article reviews the recent research progress on islet fibrosis.

A 50-year-old female was admitted to the hospital on December 6, 2009 due to "dry mouth, polydipsia for more than 1 year and confusion for 3 h". Previous history of diabetes for 1 year, irregular oral metformin, no monitoring of blood glucose levels. Three hours before admission, he was found bedridden without obvious trigger, refusing to respond to calls, and twitching in both upper limbs. Physical examination at admission showed: blood pressure 121/74 mm Hg (1 mm Hg =0.133 kPa) and pulse 104 beats/min. Laboratory tests showed: blood glucose 33.7 mmol/L, blood potassium 3.2 mmol/L, blood sodium 172 mmol/L, blood chloride 121 mmol/L, blood calcium 2.4 mmol/L, blood urea nitrogen 7.4 mmol/L, and blood creatinine 122.9 μ mol/L; Urinary specific gravity 1.005, urine occult blood 2+, urine ketone body negative, urine glucose negative; Plasma osmolality was 392 mmol/L, blood gas pH 7.4, bicarbonate 36.5 mmol/L. No abnormalities were found on CT of the head. The final diagnosis was hyperosmolar nonketotic diabetic coma. Actively replenish fluids and potassium, the fluid replenishment volume was about 9 L in 24 hours, and the urine volume reached 4.7 L in 24 hours. Monitor blood glucose and adjust insulin dosage after continuous intravenous infusion of 6 U/h insulin. The patient's consciousness gradually changed from lethargy, the convulsions of both upper limbs were relieved, and his blood sugar steadily decreased. Laboratory tests the next day showed: blood glucose 10.4 mmol/L, blood sodium 139 mmol/L, blood chloride 106 mmol/L, blood urea nitrogen 3.15 mmol/L, blood creatinine 80 μ mol/L, glycosylated hemoglobin 11.9%, urine microalbumin 14 mg/L. Fundus examination showed diabetic retinopathy stage III in both eyes. Arterial color ultrasound showed that there was no obvious sonographic image of the bilateral carotid arteries, and the intima of the arteries of both lower limbs was slightly thick and less smooth. Electrocardiogram showed: sinus rhythm, T wave changes in some leads (T_{V5, V6}Slightly lower flat). After eating a small amount, patients can be injected with ultra-short-acting insulin before 3 meals and ultra-long-acting insulin once a day. Thereafter, the patient's condition was stable and his blood sugar was well controlled. After 10 days, the biochemical examination showed that blood sodium was 162 mmol/L and blood chlorine was 120 mmol/L, so urine was taken for 24 hours to perform electrolyte examination. The patient's urine output reached 8.4 L in 24 hours. Following up the medical history, it was found that the patient's urine output had been maintained at 5~8 L/d for 18 years, and he was polydiptic without diagnosis and treatment. The results of thyroid function tests were normal. The water-free pressure test showed that the body weight was 88-92 kg, the blood pressure was 98-110/60-68 mm Hg, the urine volume was 300-400 ml/h, and the urine specific gravity was 1.005 after 8 hours of water-free pressure. After intramuscular injection of pituitrin for 5 U, the patient's blood pressure increased to 130~140/90~105 mm Hg, urine output decreased to about 100 ml/h, and urine specific gravity increased to 1.02. Cranial MRI showed: Vacuolar sella turcica. Intravenous bolus injection of desmopressin 2 μ g/d significantly reduced the patient's daily urine output by 1.4~2.4 L, blood pressure by 100~130/60~90 mm Hg, and blood sodium by 122 mmol/L, causing dizziness and other discomfort. After switching to intravenous bolus injection of 1 μ g/d desmopressin, dizziness symptoms were relieved. Blood pressure was 98-110/60-64 mm Hg, blood sodium was 135 mmol/L, and blood glucose was 5.5-7.4 mmol/L. The discharge diagnosis of the patient was: (1) diabetes, hyperosmolar non-ketotic diabetic coma; (2) Vacuolar sella turcica syndrome, central diabetes insipidus.

Inositol oxygenase (MIOX) is the first rate-limiting enzyme in the metabolic pathway of inositol, and its activity is positively correlated with blood glucose concentration. Previous studies have shown that MIOX activity and inositol levels are associated with the development of diabetic complications. The purpose of this study was to observe the association of single nucleotide polymorphism of MIOX gene with type 1 diabetes and its complications.

At present, the calculation of preprandial insulin dosage is mainly based on preprandial blood glucose and meal quantity, and less consideration is given to preprandial energy consumption. Theoretically, glycogen in liver and skeletal muscle will rise after meals, which can last for several hours; Fat intake will increase the deposition of free fatty acids in the blood and liver and skeletal muscle lipids, affecting insulin sensitivity. This study aimed to analyze the association between lunch energy intake and impaired blood glucose after dinner.

Mucinoids are acute phase-responsive proteins that reduce inflammatory responses and protect tissues. Previous studies have found that urinary mucoid secretion rate (UOER) can be used as an independent factor in early prediction of mortality in patients with type 2 diabetes.

Exercise can effectively prevent the occurrence of long-term complications of diabetes by losing weight. However, exercise can also increase the risk of metabolic disorders and cardiovascular events. This study aimed to analyze the effect of short-term exercise on the insulin response in patients with type 2 diabetes.

Early diagnosis of diabetic neuropathy is crucial to prevent long-term complications of diabetes. Existing new detection methods include circumferential diameter discrimination detector (TCD), steel ball test, automated nerve conduction examination (NCS), NeuroQuick and Neuropad.

Studies have shown that diabetic retinopathy has chronic inflammatory characteristics, and effective control of blood sugar can reduce the occurrence and development of retinopathy. However, reestablishing good glycemic control after long-term poor glycemic control does not immediately improve retinopathy. This study aimed to elucidate the role of inflammatory mediators in the development of diabetic retinopathy and the mechanisms by which retinopathy is difficult to reverse after reestablishing good glycemic control.

Diabetic neuropathy (DN) is a common diabetic complication. This study evaluated the odds of other diabetic complications and comorbidities in patients with DN and their impact on the medical costs of patients.

As we all know, diabetes can affect many aspects of patients' lives, especially for adolescents with diabetes. Social factors and peer pressure are particularly prominent in adolescence. To explore the degree of attention paid to the care of patients with diabetes in late adolescence, this study analyzed data from practice in 36 countries.

Anti-Mullerian hormone (AMH) is a member of the transforming growth factor-beta (TGF-beta) superfamily and is involved in the regulation of oocyte maturation and follicular development. Female menstrual disorders, polycystic ovary syndrome (PCOS), miscarriage and so on are closely related to energy metabolism imbalance. Insulin resistance (IR), hyperinsulinemia, hyperandrogenemia, adipocytokines, etc. may play an important role in this. IR can cause hyperinsulinemia and increase the differentiation of ovarian granulosa cells. It is speculated that IR and adipocytokines may play a certain role in the secretion of AMH by ovarian granulosa cells. This study investigated the relationship between IR and adipocytokines and AMH in non-PCOS women of childbearing age.

At present, it is still unknown whether patients with stress hyperglycemia have abnormal glucose metabolism or hormone overreaction, and whether stress hyperglycemia predicts abnormal glucose tolerance in the future is also unknown. The purpose of this study was to determine the relationship between the condition, plasma cortisol level and hyperglycemia in patients with hyperglycemic acute myocardial infarction, and the glucose metabolism status of patients after discharge from hospital.

Statistics released by the International Diabetes Federation (IDF) show that the global prevalence of diabetes was 6.0% in 2007, and the number of patients has reached 246 million. It is estimated that the number of diabetes patients worldwide will reach 380 million by 2025^[1]。 The situation of diabetes in China is also severe. In the past 20 years, with the rapid development of China's economy, the improvement of living standards caused changes in dietary structure and lifestyle, and the gradual aging of society, the prevalence of diabetes in China has increased significantly. It is estimated that there are more than 40 million diabetic patients in China^[1]。 Diabetes not only directly threatens the health of patients, causes damage to many important organs in the whole body, seriously affects the quality of life and lifespan of patients, but also greatly increases health care expenditure, causing a heavy economic burden to society and individuals. Therefore, it is very important to strengthen diabetes management, improve blood sugar control and reduce complications to reduce the burden of disease and economic burden.

obstructive sleep apnea hypopnea syndrome (OSAHS) not only easily causes multi-system damage, but also is a progressive disease, especially in obese and habitual snorers. Over time, it can gradually develop into OSAHS patients, or from mild to moderate to severe patients, with various comorbidities^[1]Even malignant production, traffic accidents or sudden sleep death occur. Only when OSAHS is treated scientifically and standardizedly, it is possible to remove the causative factors and control the multisystem damage caused by OSAHS (especially cardiovascular and cerebrovascular diseases and diabetes).

obstructive sleep apnea hypopnea syndrome (OSAHS) is a potentially harmful disease that can cause a series of complications and even death in severe cases. Its main manifestations are snoring during sleep accompanied by apnea and/or hypopnea, repeated hypoxia and hypercapnia at night, and sleep structure disorder, which in turn leads to sleepiness and memory loss during the day, autonomic nervous system dysfunction and even cardiovascular and cerebrovascular complications, multiple organ damage, etc., which seriously affect the quality of life and lifespan of patients. Further research results reveal that OSAHS itself is involved in the occurrence and development of diabetes, metabolic syndrome, coronary heart disease and stroke as an independent risk factor for many systemic diseases, and insulin resistance caused by OSAHS plays a vital role in the occurrence of these complications.

obstructive sleep apnea (OSA) is common in patients with type 2 diabetes^[1], both are clinically, epidemiologically and pathogenetically relevant and independent of obesity. At present, the harm of type 2 diabetes to health has been recognized by people, but the harm of OSA to health and the medical burden brought by it are far from being recognized by people. Therefore, it is necessary to make people realize the relationship between OSA and type 2 diabetes through the efforts of various disciplines, and take practical actions.