Volume 06 · Issue 10 · 2014

In recent years, countries around the world have strengthened the research on the prevention and treatment of diabetes mellitus and diabetic nephropathy. According to statistics, in 2013, 692 papers related to diabetic nephropathy included in SCI were published globally, including 135 in the United States, 120, 75 and 37 in China, Japan and India respectively. The number of papers in the research of diabetic nephropathy in China ranks second, which shows that the research in the field of prevention and treatment of diabetic nephropathy in China has made great progress. It is worth noting that because China is already the largest diabetic country in the world, it is also a major country with diabetic nephropathy^[1]And the proportion of patients on dialysis due to kidney failure caused by diabetes is still growing rapidly. Therefore, we need to strengthen the research on the prevention and treatment of diabetic nephropathy, especially the screening of early diabetic nephropathy.

To investigate the association between peripheral vascular disease risk and indicators of kidney function, such as glomeruar filtration rate (GFR)and urinary albumin/creatinine ratios (UACR) in type 2 diabetes patients.

We performed a cross-sectional analysis in 3 611 diabetic inpatients (male: 2 053, female: 1 558, age: 58±14) from Shanghai Diabetes Centre at Shanghai Jiaotong University-Affiliated Sixth People's Hospital from January 2011 to August 2013. Diabetes was diagnosed by 1999 WHO diabetic diagnostic criteria. Clinic parameters were collected from electronic medical records system. Peripheral vascular diseases (PVD) were diagnosed by combined carotid and lower extremity ultrasonography. GFR was estimated using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Creatinine-Cystatin C Equation. Patients were classified into five groups by GFR (GFR≥90, 75≤GFR<90, 60≤GFR<75, 30≤GFR<60 and GFR<30 ml·min^-1·1.73 m^-2 group) or three groups (0≤UACR<30, 30≤ UACR<300 and UACR≥300 mg/g) by UACR. Morbidities of PVD prevalence rate, peripheral vascular sclerosis, plaque, stenosis and occlusion was compared by ANOVA, chi-square. Meanwhile, multivariable logistic regression analysis was used to estimate the risk between different groups with kidney dysfunction (assessed by GFR and UACR) and PVD. SPSS 17.0 was used for statistical analysis and P value<0.05 were considered statistically significant.

The deteriorated albuminuria and kidney dysfunction was found correlated to increased morbidities and risks of incident peripheral vascular disease (PVD). The odd ratio(OR)s of mild peripheral sclerosis and plaques for patients with GFR 75-90 ml · min^-1· 1.73 m^-2 were 2.020(1.558-2.620) and 2.104(1.611-2.748), respectively (all P<0.01), while OR of more severe peripheral arterial stenosis and occlusion for patients with GFR 60-75 ml·min^-1·1.73 m^-2 were 2.432 (1.541-3.839) and 2.785 (1.419-5.466) (all P<0.01) when compared with GFR ≥90 ml · min^-1 · 1.73 m^-2. Meanwhile the increased risk of incident PVD with abnormal UACR could range from 49.2% to 268.1% (P<0.05).

Our study indicates that it's time to take action for early prevention of macrovascular complications once T2DM patients with UACR>30 mg/g or GFR <75 ml·min^-1·1.73 m^-2.

To investigate the relation between the treatment of diabetes and the depression in type 2 diabetes mellitus in Jiangsu Province.

All 2 953 outpatients with type 2 diabetes were surveyed with questionnaire in July 2009. The main content of the questionnaire included the demographic and metabolic data and diabetes-related health behaviors. Blood samples of the patients were collected for the assessment of glycated hemoglobin A1c(HbA1c). Diagnosis of depression(Beck depression scale): ≤4 points, no depression; 5-13 points, mild depression; 14-20 points, moderate depression; 21 points or higher, severe depression. The logistic regression analysis was used in analysis of related factors of depression.

Total of 2 741 cases were qualified for data analysis. The overall incidence of depression in the type 2 diabetics was 51.1%(1 401 cases), including 37.7%(1 034 cases) with mild, 8.5% (234 cases) with moderate and 4.9% (133 cases) with severe depression. Compared with those in patients without depression, the female gender rate(55.9% vs 44.7%), diabetes education rate(46.8% vs 38.7%), hypertension rate(46.3% vs 40.4%), diabetes complications rate(39.5% vs 29.2%) in patients with depression were all significantly higher(χ²=34.65, 18.32, 9.63, 32.12, all P<0.05), and the patients were also younger((56±11) vs (57±11) years,t=2.80, P<0.05). Logistic regression analysis revealed that female gender (OR=0.65), diabetes education (OR=1.21), diabetes treatments (OR=1.41) and complications (OR=1.15) were associated with depression(all P<0.05), no correlation was found between HbA1c and depression. The depression incidence in metformin group (42.9%) was the lowest in the patients treated with single agent. The incidence of moderate and severe depression in the patient treated with three kinds of agents was higher than those in patients treatd with single and two agents (20.1%, 10.1%, 10.4%, respectively; χ²= 12.08, 12.98, both P<0.05).

The incidence of depression is high in patients with type 2 diabetes mellitus, and female gender, diabetes education, complications, treatment and the diabetes complication is related with the depression.

To investigate the frequency and clinical characteristics of fulminant type 1 diabetes (FT1D) and to clarify the clinical significance of the subtype in pediatrics.

Case-control study designed and Data collected from hospitalized registration system. All new diagnosed type 1 diabetes (T1D) patients from January 2004 to December 2012 were enrolled. According to the diagnostic criteria, we obtained 11 FT1D cases from 853 T1D, at the same time, we match the classical type as control group according to the same gender, age(±2 years), the same season and same year with a ratio of 1∶4. We studied the clinical features, laboratory parameters and follow-up clinical outcome for at least one year in both groups.

There were 468 classical type 1 diabetes patients onset with diabetic ketosis(DK) or diabetic ketoacidosis(DKA) among 853 cases. Eleven cases (6 boys) were in line with FT1D criteria. Frequency of FT1D accounted for 1.29% of all classic T1D, and 2.35% in T1D with DK or DKA onset. Compared with the classical group, fluminant group has no statistical significance in acute severe complications, the honeymoon rate and lasting period, abnormal electrolytes and etc, except body mass index (BMI).

Frequency of FT1D below 18 years old is very low, fluminant group shows no obvious differences compared to the classical group. However, so rare FT1D cases, we must do further study in the future to explore the clinical significance of this subgroup in pediatrics.

To investigate the association between sleep disorder and islet α-cell and βcell function in patients with type 2 diabetes.

Four hundred and forty patients with type 2 diabetes treated from July 2011 to July 2013 were divided into two groups according to Pittsburgh Sleep Quality Index(PSQI): patients without sleep disorder and patients with sleep disorder. The blood glucose and glycated hemoglobin A1c(HbA1c) was detected in the two groups. Oral glucose tolerance test(OGTT), insulin releasing test and glucagon releasing test were performed to investigate the differences of the β-cell function, glucagon and glucagon/insulin ratio between groups after fasting and glucose-load. The correlation and regression analysis were performed between PSQI and other indicators.

The level of HbA1c, fasting plasma glucose, fasting plasma insulin and HOMA-IR were significantly higher in patients with sleep disorder compared to those in patients without sleep disorder(8.6%±2.4% vs 7.5%±1.9%, (8.5±2.1) vs (6.7±1.3) mmol/L, (14.4±4.4) vs (12.9±4.6) mU/L, 5.2±1.0 vs 3.8±1.0, t=5.358, 11.085, 3.578,14.448, all P< 0.05). Insulin sensitivity index(ISI) was lower in patients with sleep disorder than that in patients without sleep disorder(-4.3±0.9 vs-4.0±0.6,t=3.379, P<0.05). There was no significant differences in basal and early-phase insulin secretion between the two groups, while the insulin area under curve was higher in patients with sleep disorder than that in petients without(t=2.489, P<0.05). Blood glucagon, area under curve of glucagon and glucagon/insulin ratio were significantly higher in patients with sleep disorder than those in patients without(t=2.047-8.131, P<0.05). Multiple stepwise regression analysis showed that PSQI score was positively related to glucagon/insulin ratio, HOMA-IR and age(β =0.244,0.281,0.307, allP<0.05), and negatively related to ISI (β =-0.105,P<0.05).

Sleep disorder is associated with the dysfunction of islet α-cells and β-cells. Improving sleep disorder may help to reduce the"dawn phenomenon"and optimize glycemic control.

To investigate the relationship between plasma fibroblast growth factor 21 (FGF-21) levels and body mass index(BMI), plasma glucose, plasma insulin levels, as well as other factors in newly diagnosed type 2 diabetes mellitus (T2DM).

180 subjects who visited Department of endocrinology, Chaoyang Hospital, Capital Medical University from January to July in 2013 were enrolledand divided into newly diagnosed T2DM group (DM group, n=136) and Impaired glucose tolerance (IGR group, n=44). We selected 52 healthy volunteer as control group (NCM group). Plasma FGF-21 levels were determined by ELISA. The association between plasma FGF-21 levels and BMI, plasma glucose, blood lipids, plasma insulin levels, homeostasis model assessment of insulin resistance (HOMA-IR), homeostasis model assessment of insulin sensitivity index(HOMA-ISI) and other factors were also analyzed. We use independent-samples t test, Pearson's correlations, multivariate linear regression analysis.

Plasma FGF-21 levels in newly diagnosed T2DM patients were significantly higher than those of healthy individuals (319.2±2.5 vs 223.09±1.43, t=2.804, P<0.05). Plasma FGF-21 levels positively correlated with triglyceride (TG) in newly diagnosed T2DM patients and healthy individuals (r=0.26, 0.38, respectively, P< 0.05 all above). Plasma FGF-21 levels positively correlated with BMI in IGR group (r=0.33, P<0.05). Multiple regression analysis suggested that HOMA-ISI was an independent related factor influencing plasma FGF-21 levels.

FGF-21 in newly diagnosed T2DM patients is associated with triglyceride levels, insulin resistance.

To investigate the relationship between serum dipeptidyl peptidase 4 (DPP-Ⅳ) and body fat content and distribution in type 2 diabetes (T2DM).

A total of 40 T2DM inpatients treated in Department of Endocrinology of the First People's Hospital of Yunnan Province from July 2013 to November 2013 were enrolled. The height, weight, body mass index (BMI) were measured; total cholesterol(TC), triglyceride(TG), low density lipoprotein cholesterol (LDL-C) were detected by electrochemiluminescence assay and serum DPP-Ⅳ were detected by enzyme linked immunosorbent assay (Ray Biotech). Body fat content and lean mass was measured by dual energy X-ray (DEXA). Based on BMI, the subjects were divided into 2 groups: the normal weight group (BMI 18.5-24.0 kg/m², NC group, n= 14) and the over weight/obese group (BMI≥24.0 kg/m², OB group, n=26). Two-tailed independent samples t test was used for comparison of normally distributed measurement data between groups. Spearman correlation coefficient was used for correlation analysis.

Compared with NC group, the level of DPP-Ⅳ in OB group was significantly higher ((765±72)vs(706±91)μg/L,t=2.2480, P<0.05). The level of serum DPP-Ⅳ was positively correlated with body fat content (FAT,r=0.498, P<0.05). The level of DPP-Ⅳ was positively correlated with trunk fat content, arm fat content and thigh fat content (r=0.567, 0.391, 0.344, respectively, all P<0.05). There was no significant correlation between the level of DPP-Ⅳ and lean body mass.

The level of serum DPP-Ⅳ may be correlated with body fat content and distribution in T2DM.

To observe the effects of continuous positive airway pressure(CPAP) treatment on inflammation and insulin resistance in patients with type 2 diabetes mellitus(T2DM) and obstructive sleep apnea-hypopnea syndrome (OSAHS).

Seventy-four patients (51 males and 23 females, with an age range of 45-66 years old) diagnosed as T2DM and OSAHS syndrome from January 2012 to January 2014 were randomly and equally divided into the treatment group(n=37) and the control group(n= 37). Patients in the treatment group were treated with CPAP for 14 days. The fasting blood glucose (FBG), fructosamine (FMN), fasting insulin (FINS), white blood cell (WBC)count, high sensitive C reactive protein (hs-CRP), hypoxia inducible factor-1α(HIF-1α) and soluble vascular cell adhesion molecule-1(sVCAM-1) was detected before and after treatment. The homeostasis model assessment (HOMA) insulin resistance (HOMA-IR) index, the mean pulse oxygen saturation (MSpO₂), the lowest pulse oxygen saturation (LSpO₂) and apnea hypopnea index (AHI) were monitored by polysomnography (PSG) before and after treatment. T test, χ ² test and Spearman correlation analysis were used to evaluate the data.

Compared to the control group, the level of FBG, FMN, FINS, MSpO₂, LSpO₂, AHI was improved in the treatment group by a certain degree after treatment(t =-123.761-120.676, all P<0.05). The level of hs-CRP, HIF-1α, sVCAM-1 and HOMA-IR was significantly reduced from(7.3±0.3)mg/L, (275±53) ng/L, (717±73) ng/L and 3.7±0.2 before treatment to(2.4±0.4)mg/L, (211±6) ng/L, (589±57) ng/L and 2.1±0.7 after treatment, respectively(t= -53.046, -19.827, -12.827, -28.342, respectively, all P<0.05). The improvements showed by Pearson analysis in HOMA-IR after treatment were positively correlated with HIF-1α and sVCAM-1 improvements (r=0.87, 0.86, both P<0.05).

CPAP may improves the inflammation status, sleep quality, insulin resistance in patients with T2DM and OSAHS.

To explore the relationship between the measures of adiposity and the prevalence of diabetes mellitus in adults of Jiangsu province.

Total of 8 400 inhabitants aged 18 years and above were selected from 14 chronic no-communicable diseases surveillance areas by multi-stage cluster random sampling method in Jiangsu province. Information of the inhabitants was collected with a questionnaire survey, anthropometric measurement and biochemical test of blood. Data was analyzed to explore the relationship between obesity, central obesity, the measures of adiposity including weight, body mass index(BMI), waist circumference, waist-height ratio and the prevalence of diabetes mellitus by unconditional logistic regression analysis.

The prevalence of diabetes mellitus, obesity and central obesity was 8.5%, 13.6%, 30.8% respectively in adults of Jiangsu province. The distributional difference of the prevalence of diabetes mellitus in different age groups was statistically significant (χ²= 119.77, P<0.05). The prevalence showed an obvious rising trend with age growth. The results of unconditional logistic regression analysis showed that obesity, central obesity, weight, BMI, waist circumference and waist-height ratio were associated with diabetes mellitus(χ²=39.01, 86.82, 95.11, 114.61, 119.76, all P<0.05). The risk of diabetes mellitus was rising with the increase of BMI, waist circumference and waist-height ratio. About 1-unit greater measures of BMI, waist circumference and waist-height ratio were respectively associated with 13% (OR=1.13, 95%CI:1.10-1.15), 5% (OR=1.05, 95%CI:1.04-1.06) and 8% (OR=1.08, 95%CI:1.07-1.10) higher risk of diabetes mellitus. And about 1-SD greater measures of waistheight ratio, waist circumference and BMI were respectively associated with 62% (OR=1.62, 95% CI:1.49-1.76), 61% (OR=1.61, 95% CI:1.48-1.75) and 49% (OR=1.49, 95% CI:1.38-1.62) higher risk of diabetes mellitus. The risk of diabetes mellitus increased in turn with the influence of BMI, waist circumference and waist-height ratio.

The BMI, waist circumference and waist-height ratio were closely associated with the prevalence of diabetes mellitus. Obesity is the important factor with great influence on the prevalence of diabetes mellitus. The prevalence of diabetes mellitus will increase with increased obesity degree.

To explore the effect of stromal cell-derived factor-1α(SDF-1α) on extracellular matrix (type Ⅳ collagen) in human renal proximal tubular epithelial cells (HKC) with the different glucose conditions.

HK cell were cultured exposed to SDF-1α and transform growth factor-β1(TGF-β1) of the different concentration with normal (NG group: 5.5 mmol/L glocuse) or high (HG group:25.0 mmol/L glucose) glucose. With the stimulation of TGF-β1 and SDF-1α for 12 hours later, the HKC were divided to the following groups: control group(NC group), S group (SDF-1α alone),T group (TGF-β 1 alone),S+T group(SDF-1α and TGF-β1 together). Real-time PCR and Western blotting were used to detect the m RNA and protein expression of type Ⅳ collagen in HKC. Comparison between two groups was usingt test.

(1)The m RNA expression of SDF-1α and CXCR4 mRNA was detected continuously in HKC. High glucose could increase the expression of SDF-1α and CXCR4 mRNA in HKC with a time-dependent manner, which reached the highest level at 24 h. The mRNA level of CXCR4 at 24 h was 1.2 times of those at 12 h(t=6.08, P<0.05), meanwhile the mRNA level of SDF-1α at 24 h was 1.58 times of those at 12 h(t= 7.52, P<0.05). (2)With high glucose SDF-1α suppressed the mRNA and protein expression of type Ⅳ collagen induced by TGF-β1 in HKC. The mRNA and protein expression level of type Ⅳ collagen in S+T group were 0.33 times(t=12.57, P<0.05), and 0.47 times(t=14.23,P<0.05)of those in T group, respectively. Under the normal glucose condition, SDF-1α had no effect on the expression of type Ⅳ collagen induced by TGF-β1.(3)TGF-β1 stimulated mRNA and protein expression of type Ⅳ collagen in HKC, especially in high glucose. The mRNA and protein expression level of type Ⅳ collagen in T group were 6.63 times(t= 19.21, P<0.05),and 2.59 times(t=15.71, P<0.05)of those in control group respectively.

(1) SDF-1α maybe attenuate the renal fibrosis by suppressing the expression of type Ⅳ collagen induced by TGF-β1 in high glucose.(2)TGF-β1 promotes the development of DN by increasing the expression of type Ⅳ collagen in HKC.

To investigate the protective role of oridonin in the vascular endothelial cells dysfunction induced by high glucose and lipid.

The optimum concentration of oridonin on human umbilical vein endothelial cells(HUVECs)were determined by MTT assay.The model of HUVECs was established and divided into 3 groups:control group,oridonin group(oridonin treated for 24 h,with high glucose and high palmitic),high glucose and palmitic acid group 33.3 mmol/L glucose.HUVECs were pretreated with oridonin under the condition of 33.3 mmol/L glucose and 500 μmol/L palmitic acid,while other groups received 33.3 mmol/L glucose and 500 μmol/L palmitic acid and dimethyl sulfoxide(DMSO). After 48 h treatment,the concentration of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in the supernatant was detected by the enzyme-linked immunosorbent assay (ELISA) to observethe inflammation state while flow cytometry was used to detect the cell apoptosis of each group,the mRNA expression of TAp63 and Silent information regulator 1 (Sirt1) in HUVECs was detected by the real time polymerase chain reaction(real time PCR). And the protein expression of TAp63,Sirt1,phosphorylated extracellular regulated protein kinases (p-ERK) and B-cell lymphoma 2(Bcl-2) were determined by Western-blotting.

The optimum concentration of oridonin treating on HUVECs was 5 μmol/L when effect for 24 h. Compared with the control group,the apoptosis rate,the protein expression of phosphated ERK, and the concentration of inflammation factors(TNF-α and IL-6) in the supernatant were significantly higher( t=14.34,12.59,17.37, 17.90, P<0.05 all above)while the expression of TAp63 mRNA and protein,Sirt1 mRNA and protein,Bcl-2 protein was significantly lower in the HUVECs in the high glucose and palmitic acid group(t=-22.50,-6.02,-16.22,-6.72,-7.71,all P<0.05).But in the oridonin group which were treated with 33.3 mmol/ L glucose and 500 μmol/L palmitic acid, the pretreatment with oridonin significantly induced the expression of TAp63 mRNA and protein(t=5.85,5.06,all P<0.05),Sirt1 mRNA and protein level(t=4.55,3.04, all P<0.05)and Bcl-2 protein(t=5.81,P<0.05).Furthermore, the apoptosis rate,the protein expression of phosphated ERK, and the concentration of TNF-α and IL-6 in the supernatant were significantly reduced(t=-7.11,-7.81,- 10.51,-10.36,all P<0.05).

Oridonin could protect vein endothelial cells from the damage induced by high glucose and palmitic acid,which may be related to the inhibition inflammation induced by high glucose and palmitic acid,or to increasing the expression of TAp63,Sirt1,Bcl-2 and decreasing the expression of p-ERK.

To investigate the clinical features and mitochondrial mutation for a female diabetes patient with overt neural hearing loss and literature review. A female diabetes patient with overt neural hearing loss was hospitalized in the endocrine section of our hospital from 2009 to 2013. We retrospected her clinical data, and detected the mitochondrial mutation for the proband and her family members. The prob and presented symptoms of emaciation, dark skin, poor resistance, islet function decrease, blood lactate levels elevation, normal glomerular filtration rate, hematuresis continued presence, and combined with intestinal polyps and arrhythmia. Most of the families suffered from diabetes mellitus, the mother of the proband died of diabetic complications. One of the proband' s brothers diagnosed as diabetes mellitus with mildly decreased hearing; another brother was healthy; her daughter had mildly hearing defect but normal blood glucose. Mitochondrial 3243A→G mutation was detected in the proband and the members with hearing defect. The diabetic patient who presents the hearing defect and elevated lactic acid levels should be significantly suspected of mitochondrial diabetes. Gene sequencing is helpful to diagnose of mitochondrial diabetes.

diabetic nephropathy (DN) is a common chronic complication of diabetes and the leading cause of end-stage renal disease in developed countries. However, the prevention and treatment of DN is still a major problem today. Incretins are new hypoglycemic drugs, including GLP-1 analogs/receptor agonists that mimic the action of glucagon-like peptide-1 (GLP-1) or activate GLP-1 receptors, and dipeptidyl peptidase-IV (DPP-IV) inhibitors that inhibit the degradation of GLP-1. In addition to good hypoglycemic efficacy, these drugs are also widely used in clinical practice due to their lower risk of hypoglycemia and less weight gain. In addition, many basic or clinical studies have also confirmed that incretin treatment may have renal protective effects in addition to protecting islet β cell function, inhibiting inflammatory response, and reducing oxidative stress. In this paper, the progress of the role of incretin drugs in DN is reviewed.

Insulin has the function of regulating carbohydrate and fat metabolism. Insulin stimulates glucose uptake and utilization in peripheral tissues by activating protein kinase, inhibits glycogenogenesis and glycogenolysis; Accelerate the synthesis of fatty acids from liver glucose and inhibit lipolysis. The main pathogenesis of type 2 diabetes mellitus (T2DM) is insulin resistance (IR) in liver, skeletal muscle and adipose tissue. The number of diabetic patients worldwide reached 366 million in 2011, and it is expected to increase to 552 million by 2030, of which T2DM accounts for about 90%^[1]。 The exact mechanisms of IR and T2DM are not fully understood, but there is substantial evidence that oxidative stress plays an important role in their development^[2,3]。

Dehydroepiandrosterone (DHEA) and its sulfateester (DHEAS) are the most abundant steroid hormones in human blood circulation, which are mainly synthesized by cytochrome P450c17 in the reticular zone of adrenal cortex. In the body, most of DHEA exists in the form of sulfide, and its sulfate group can bind to plasma protein to protect it from the degradation of hepatocytes. Therefore, DHEAS exist in the body for a longer time than DHEA, and the metabolic clearance rate is slower. The regulation of cell metabolism by DHEA and DHEAS depends on different cell types, target tissues, and species. DHEA is a precursor of androgen and estrogen. DHEA is converted into androgen or estrogen in peripheral tissues, and exerts indirect biological effects in the form of intracellular secretion. Recent studies have found that in women, estrogen maintains energy balance by suppressing energy intake and fat formation, promoting energy expenditure, and improving insulin secretion and insulin sensitivity. In men, testosterone works by converting to estrogen, inhibiting fat accumulation and improving insulin sensitivity^[1]。 In ovariectomized female rats, DHEA intervention was able to reverse high-fat diet-induced insulin resistance and restore insulin sensitivity^[2]。 A randomized controlled trial in an elderly population (57 men and 68 women) showed that DHEA intervention (50 mg/d, 2 years) was able to reduce triglyceride levels and significantly reduce abdominal fat accumulation and decrease the area under the oral glucose tolerance curve, all suggesting that DHEA could improve insulin sensitivity^[3,4]。 Therefore, we conclude that DHEA/DHEAS has the potential to develop into an important biomarker of diabetes and metabolic diseases in the future. This review will provide an overview of the research progress of DHEA antidiabetic effects.

A 38-year-old male was admitted to the hospital due to elevated blood sugar for 14 years and repeated skin ulcers on both feet for 2 years and aggravated for half a year. The patient was diagnosed with type 2 diabetes mellitus (T2DM) after physical examination 14 years ago with fasting blood glucose of 12 mmol/L, oral glucose tolerance test (OGTT) 2 h blood glucose of 25 mmol/L and glycosylated hemoglobin (HbA1c) of 12.5%. After intensive insulin therapy, it was changed to oral hypoglycemic drugs, and usually only intermittently purchased hypoglycemic drugs. Has a history of drinking alcohol, about 500 ml per week, and no history of smoking.

Currently diabetic foot (DF) is the leading cause of non-traumatic amputation. Ischemia, neuropathy and infection are considered to be the most critical factors in the development of DF ulcers. Although the treatment of DF has made great progress, the healing of patients with DF complicated infection is still poor, which may be related to factors such as delayed diagnosis, complicated peripheral arterial disease (PAD), infection with multi-drug resistant bacteria, and osteomyelitis. The pathogens of DF complicated infection were mainly influenced by the characteristics of DF ulcer (course, area, depth), early antibiotic use and PAD, but such indicators could not reliably predict the types and burden of pathogens. Therefore, it is necessary to clarify the influencing factors of microbial burden in DF ulcer complicated with infection.

Diabetic foot ulcers are the most common cause of hospitalization in diabetic patients. Even under current standard treatments, non-healing ulcers can lead to amputation, seriously damaging the patient's health and imposing a huge financial burden. Therefore, there is an urgent need to develop clinical treatment methods for non-healing diabetic foot ulcer. The application of mesenchymal stromal cells (MSCs) is a novel therapeutic approach. Previous studies have proved that MSCs can promote vascular regeneration, granulation formation and ulcer healing. However, intravenous infusion of MSCs can affect the efficacy of MSCs due to intravascular cell death and low local cell load of ulcer.

Diabetic foot infection (DFI) is one of the common complications of diabetic patients, its incidence rate is as high as 58%, and it is also an important cause of hospitalization of diabetic patients. At present, there is no unified anti-infection regimen for DFI in the world. The choice of antibiotics is mainly based on clinicians' experience, the severity of infection and the pathogenic bacteria. Since the most common pathogen is Staphylococcus aureus, the most commonly used anti-infection regimen is narrow spectrum antibiotics targeting aerobic Gram-positive, while broad spectrum antibiotics are generally used in DFI with severe infection or combined ischemia. For some patients with moderate DFI, an appropriate anti-infective regimen can avoid further hospitalization.

Diabetic foot ulcer is one of the most serious complications of diabetes, which often greatly increases the amputation rate of diabetic patients. Uric acid is the end product of purine metabolism in humans, and some current evidence suggests that elevated serum uric acid concentrations may play a key role in diabetic complications. However, it remains unclear whether hyperuricemia is a detrimental factor in diabetic foot ulcers. A team of researchers from the Department of Endocrinology, Nanfang Hospital affiliated to Southern Medical University conducted a retrospective study to investigate the relationship between elevated blood uric acid levels and the occurrence of diabetic foot ulcers in Chinese patients with type 2 diabetes.

Diabetic foot is a foot ulcer formed by a combination of neuropathy, ischemia and infection. It is one of the serious complications of diabetes. It often occurs repeatedly, takes a long time to treat, and the ulcer wound is difficult to heal. At present, there is no ideal treatment method, which is the main cause of disability caused by amputation. It has been believed that hyperbaric oxygen therapy can achieve good curative effect in the treatment of hypoxia and ischemic diseases, or a series of complications caused by hypoxia and ischemia; And for some serious infectious diseases and autoimmune diseases, hyperbaric oxygen therapy can also achieve better results. However, the latest research results show that hyperbaric oxygen therapy does not seem as ideal as people expect for patients with diabetic foot ulcers.