Volume 03 · Issue 04 · 2011

Diabetic foot is one of the common chronic complications of diabetes, which imposes a heavy burden on socioeconomy. Diabetic foot ulcers accounted for more than 33% of the medical expenses for diabetes in the United States in 2007, which amounted to $116 billion^[1]。 Although there is no national data on diabetic foot disease including medical expenses in China, recent surveys show that diabetic foot ulcer has become the main cause of chronic ulcer among hospitalized patients in China, and the proportion of chronic foot ulcer patients has increased from 4.9% in 1996 to 33.0% in 2008^[2]。 The prognosis of diabetic patients after amputation is poor, Li Xiang et al.^[3]It was reported that the mortality rate of patients 5 years after amputation was close to 40%. Therefore, the prevention and treatment of diabetic foot has important clinical significance. The successful experience of diabetic foot prevention and treatment and the decline of amputation rate in foreign countries tells us that three basic principles should be implemented in the prevention and treatment of diabetic foot, namely professional treatment, multidisciplinary cooperation and prevention.

Diabetic foot ulcers and their resulting amputations are one of the leading causes of disability and death in diabetic patients. Statistics show that about 15% of diabetic patients develop lower limb ulcers during their course of disease^[1,2]With an estimated incidence of 0.5% to 3.0% per year^[3,4]Among them, 7% to 20% of patients with diabetic foot ulcer need amputation, while 85% of lower limb amputations in diabetic patients are caused by foot ulcer^[5,6]。 Diabetic foot ulcer is a kind of refractory wound. With the development of science and technology and the deepening of people's understanding of diabetic foot ulcer, dressings applied to various wounds in different states have appeared. Faced with various modern dressings of different materials, many untrained medical staff may feel at a loss, so they have to continue to apply traditional methods for treatment. This is also one of the reasons why many modern dressings can't be popularized.

The concept of diabetic foot was first proposed by Oakley in 1956, and in 1972 Catterall defined it as a foot with loss of sensation due to neuropathy and loss of vitality due to ischemia combined with infection. The World Health Organization defines diabetic foot as: foot infections, ulcers, and/or deep tissue destruction associated with distal nerve abnormalities of the lower extremities and varying degrees of peripheral vasculopathy. With the deepening of people's understanding of diabetic foot, it is now considered that diabetic foot is a group of foot syndromes, rather than a single symptom. It should have at least three elements: (1) be diabetic; (2) There are defects or lesions in tissues below the ankle (ulcers or gangrene); (3) Accompanied by certain neurological and/or vascular lesions of the lower limbs. This article briefly discusses the progress of surgical treatment of diabetic foot.

At noon on June 26, 2011, the San Diego International Convention and Exhibition Center was packed. Professor Barbara E. Corkey, winner of the Banting Award for Medical Science Achievement at the 71st Annual Meeting of the American Diabetes Society (ADA) and director of the Center for Obesity Research at Boston University School of Medicine, USA, gave a lecture on "Hyperinsulinemia, is it a cause or an effect?" with a novel topic and rich content, challenging the traditional view and proposing a new concept of hyperinsulinemia as the cause of type 2 diabetes. The wonderful academic report has deeply attracted more than 10,000 diabetes scholars from all over the world.

To investigate the plantar pressure distribution changes in type 2 diabetic patients with peripheral neuropathy.

From January 2004 to December 2009, a total of 1103 patients with type 2 diabetes were enrolled and divided into diabetic peripheral neuropathy (DPN) group (n=301) or diabetic control (DC group, without DPN) group (n=802). Demographic characteristics were recorded. The lipid profile, fasting plasma glucose (FPG), hemoglobin A1c (HbA1c) and urinary albumin excretion rate (AER) were measured. Plantar pressure was recorded with the EMED-AT system by the"First Step Approach", and the parameters were calculated by EMED software. Independentt-test or Mann-Whitney U test was applied in the data analysis.

The patients in the DPN group had statistically higher age, waist-to-hip ratio, systolic blood pressure, FPG, HbA1c and urinary AER as compared with those in DC group (all P<0.05). There was no significant differences in the plantar peak pressure (PP) between the two groups (P>0.05). However, the contact time (CT) ((1484±412) vs (1241±281)ms,t=-9.414, P<0.05), pressure-time intergrals (PTIs) ((333±115) vs (278±89) kPa·s,t=-7.446, P<0.05) and force-time intergrals ((628±187) vs (536±149) N·s,t=-7.707, P<0.05) increased significantly in DPN group in comparison with those in DC group. Compared to DC group, the peak pressure in heel (rear foot) ((396±101) vs (411±105) kPa,t=2.163, P<0.05), the second metatarsal ((240±87) vs (269±95) kPa,t=4.563, P<0.05)or third metatarsal ((241±75) vs (262±77) kPa,t=4.046, P<0.05) decreased, while the peak pressure in foot arch (midfoot) ((122±48) vs (115±31) kPa,t=-2.487, P<0.05), the fifth metatarsal ((218±116) vs (195±99) kPa,t=-3.131, P<0.05), and the third-to-fifth toes ((108±50) vs (98±46) kPa,t=-3.315, P<0.05) increased in DNP group. The PTIs in rearfoot ((228±100) vs (189±67)kPa·s,t=-6.201, P<0.05), midfoot ((82±45) vs (66±26) kPa·s,t=-6.151, P<0.05), and in each mask of whole forefoot plantar were higher in DNP group than those in DC group.

DNP patient has an abnormal plantar pressure distribution and a longer contact time. Increasing of PTIs, induced by a synergistic effect of both plantar pressure and contact time, may play a key role in the development of diabetic foot ulcer.

To investigate the microbiological profile and antibiotic susceptibility patterns of organisms isolated from diabetic foot ulcers.

A retrospective study was carried out on the microbiological profile and antibiotic susceptibility in 532 strains of pathogens isolated from 358 patients with diabetic foot ulcers in West China Hospital from January 1996 to December 2009. The data between groups was compared by using χ ² test.

Foot infection occurred in 507/662 (76.6%) patients with diabetic foot. A total of 532 strains of pathogens were isolated from foot ulcers in 358/510(70.6%) patients. Gram-positive aerobes were most frequently isolated (51.4%, 281 strains), followed by gram-negative aerobes and fungus (38.7% and 8.5%, 206 and 45 strains, respectively). One hundred and thirty-six patients (26.6%) showed polymicrobial involvement. Among the 281 strains Gram-positive bacteria, 89 (16.7%) strains were Staphylococcus aureus, 48(9.0%) strains were Enterococcus, and 43(8.1%) strains were Staphylococcus epidermidis, including three strains of vancomycin resistant Enterococci(VRE) and ten strains of methicillin resistant Staphylococcus aureus(MRSA). Gram-positive bacteria were highly resistant to aztreonam (87.7%), erythromycin (83.5%), ceftriaxone (83.2%) and penicillin (81.0%); vancomycin and norfloxacin were the most effective agents against gram-positive bacteria. Among the 206 strains gram-negative bacteria, 34 strains (6.4%) were Escherichia coli, 23 strains (4.32%) were Enterobacter cloacae, 21 strains(3.9%) were Proteus vulgaris. Gram-negative bacteria were highly resistant to ampicillin(90.2%), ampicillin/sulbactam (75.3%), rifampicin (72.5%), penicillin (66.7%) and erythromycin (60.8%); Imipenem, amikacin sulphate and cefpodoxime were the most effective agents against gram-negative bacteria. The major fungus was Blastomyces albicans (2.4%, 13 strains).

Gram-positive aerobes are the predominant pathogens isolated from diabetic foot ulcers compared with gram-negative bacteria. Vancomycin and imipenem still keep highly antibacterial activity. It is very important to pay attention to pathogens survey and use antibiotics more rationally.

To evaluate the efficacy of beraprost sodium in the treatment of diabetic peripheral artery disease.

Thirty diabetic patients with peripheral artery disease treated from November 2009 to August 2010 were randomized into two groups in the ratio of 2 to 1: the group A treated with beraprost sodium(40 μg tid, n=20) and the group B with aspirin (100 mg qd, n=10)for 12 weeks. The pain-free walking distance (PFWD), maximum walking distance (MWD) were measured at 0 week (before treatment), 12 week (after treatment) and 24 week (12 weeks follow-up after treatment). Ankle-brachial index (ABI) and metabolic data were evaluated at 0 and 12 week. The t, χ ² and rank test was used in the data analysis.

No differences in age, gender and diabetic complications was found between two groups. Ischemic symptoms were significantly improved in group A than in group B (90.0% vs 50.0%, χ ²=5.96, P<0.05). Compared with those at baseline(276 and 1000 meters), the PFWD was 350 meters(Z=-2.94, P<0.05), 315 meters (Z=-2.88, P<0.05)and MWD was 1713 meters(Z=-3.73, P<0.05), 1600 meters (Z=-3.58, P<0.05)at 12 weeks and 24 weeks respectively in group A; and it was 400 meters(Z=-2.13, P<0.05), 390 meters (Z=-0.81, P>0.05)and 1075 meters(Z=-2.54, P<0.05), 1025 meters(Z=-0.21, P>0.05) at 12 weeks, 24 weeks respectively in group B. No significant differences in the PFWD was found at baseline, 12 weeks and 24 weeks between two groups. But the absolute increased PFWD was 125 meters for group A and 30 meters for group B at 12 weeks(Z=-2.87, P<0.05); 82.5 and 0 meters at 24 weeks in group A and group B(Z=-3.31, P<0.05). The absolute increased MWD was 500, 50 meters (Z=-3.20, P<0.05) and 300, 10 meters (Z=-3.02, P<0.05) at 24 weeks in the group A and B, respectively. No significant side reaction of the beraprost treatment in these two groups.

Beraprost can be used effectively and safely in the treatment of diabetic artery disease.

To investigate the efficacy and safety of exenatide versus biphasic insulin aspart 30(BIAsp30) in patients with inadequately glycemic controlled and obese type 2 diabetes with oral antidiabetes agents.

A single center, randomized, open-label, parallel-group study was conducted. Four weeks run-in period and 16 weeks treatment period were included. Eighty subjects were enrolled((>35 years old, BMI>25 kg/m²), waist circumference(male>90 cm and female>85 cm), HbA1c 7.5%-10.5%). All subjects which received metformin (at least 1000 mg/d) or sulfonylurea (at least half the maximal dose) for at least 12 months were randomly assigned to exenatide group(n=40) or BIAsp30 group(n=40) twice or thrice daily.The t and χ ² test was used in the data analysis.

Compared to the baseline, the HbA1c values decreased in exenatide group(7.6%±0.9%)and in BIAsp30 group(7.2%±1.0%)after 16 weeks treatment(t=-3.6, P<0.01). The proportion of patients which HbA1c less than 6.5% was 37.8%(BIAsp30 group) and 16.7%(exenatide group, χ²=4.1, P<0.05). The proportion of patients which HbA1c less than 7.0% was 47.2% and 54.1%, respectively(χ²=0.3, P>0.05). Weight gain was observed for the BIAsp30 group (2.7±1.4) kg while weight loss was reported for the exenatide group (3.4±1.7) kg. The amount of subjects reporting hypoglycemic events was significantly greater in BIAsp30 group than in exenatide group (4.88 vs 1.95 events/subject per year). The reductions of systolic blood pressure, and the improvement of lipid profile in exenatide group were superior to that of BIAsp30 group. However, There was no significant difference on diastolic blood pressure and homocysteic acid between the two groups (P>0.05).

Eexenatide is superior on reduction of hypoglycemic events, control weight, and improvement of lipid parameters to BIAsp30.

To investigate the clinical heterogeneity of type 1 diabetes mellitus (T1DM) at onset.

A total of 205 newly diagnosed T1DM patients discharged from the hospital between January 1999 and December 2009 were retrospectively reviewed. Clinical characteristics and laboratory data at onset were compared among fulminant type 1 diabetes (FT1DM) and those with duration of symptoms before diagnosis shorter (acute-onset) or longer (slow-onset) than 3 months. Antibodies to glutamic acid decarboxylase (GADA) were determined by enzyme-linked immunosorbent assay (ELISA), while islet cell antibodies (ICA) , insulin autoantibody(IAA) and serum C-peptide were detected using radioimmunoassay (RIA). Statistical analyses were performed using One-way ANOVA and two independent samples t-test for measurement data, multivariate Chi-square and Fisher's exact probability test were used for enumeration data.

The proportions of FT1DM, acute-onset and slow-onset T1DM were 8.8%, 66.8%, 24.4% respectively. The onset of FT1DM was so abrupt that the concentration of plasma glucose was prominently elevated ((31±12) vs (25±10), (24±8) mmol/L, F=4.462, P<0.05), whereas HbA1c was disproportionately near normal ((6.8±1.1)% vs (12.3±2.4)%, (13.9± 2.7)%,F= 54.661, P<0.05). Ketoacidosis was almost inevitable at diagnosis (93.8% vs 45.3%, 8.0%,F= 44.943, P=0.000) and the accompanied metabolic derangement. Hyponatremia, hyperkalemia, acidosis, association with liver and kidney dysfunction was more severe in FT1DM group. Association with pregnancy was more frequent as compared to the other 2 groups (22.2% vs 0, 0, χ ²=20.982, P=0.000). Patients with slow-onset type were relatively older and had greater BMI but lost more weight at diagnosis. The post-load C-peptides were relatively higher( (0.40±0.36) vs (0.10±0.13), (0.34±0.26) nmol/L, F=8.752, P<0.05) in this group. Children and adolescents constituted a greater proportion in the acute-onset T1DM group, and the clinical characteristics were similar to the adult-onset counterpart.

Clinical heterogeneity in the 3 groups is apparent, which might indicate different mechanisms that trigger the development of T1DM leading to the phenotypic discrepancy.

To study the change of vitamin D in newly diagnosed type 2 diabetes mellitus (T2DM), and to explore the relationship between the level of serum vitamin D and islet β cell dysfunction as well as insulin resistance.

Fasting serum 25-hydroxyvitamin D₃ (25-(OH)D₃) concentration was measured by high pressure liquid chromatography (HPLC) in 97 newly diagnosed T2DM patients (men 57, women 40, aged (52±10)years) and 69 healthy controls (men 40, women 29, aged (50±11)years). Oral-glucose-tolerance test was performed, and area under the curve of glucose (AUCG), area under the curve of insulin (AUCI), early-phase insulin secretion index (ΔI₃₀/ΔG₃₀), β cell function index (HOMA-B), insulin resistance index (HOMA-IR) were compared between T2DM with low 25-(OH)D ₃ ((25-(OH)D₃ <37.5 nmol/L, n=61) and those without (n=36). The correlation of serum 25-(OH)D₃ with sex, age, body mass index (BMI), waist-hip rate (WHR), blood pressure, lipids, HbA1c, insulin resistance and β cell function was analysed by using Pearson correlation and multiple stepwise regression analysis.

The level of serum 25-(OH)D₃ was much lower in T2DM patients than in controls ((36±19)nmol/L vs (80±26) nmol/L, t=-13.00, P<0.01). The prevelence of hypovitaminosis 25-(OH)D₃ in T2DM was 62.9% (61/97). Among T2DM, when compared with those without hypovitaminosis 25-(OH)D₃, patients with hypovitaminosis 25-(OH)D₃ showed higher HbA1c and AUCG ((10.1±3.0)% vs (7.7±2.6)%, (32±7) h·mmol^-1·L^-1vs (25±7) h·mmol^-1·L^-1,t values were 4.44 or 4.45, both P<0.01), although HOMA-B, ΔI₃₀/ΔG₃₀, and AUCI were significantly lower (21±16 vs 75±64, 1.9±1.9 vs 8.3±7.7, (30±21) h·mU^-1·L^-1vs(104±80) h·mU^-1·L^-1,t values were -5.68, -6.81, and -7.69; all P<0.01). In multiple stepwise regression analysis, ΔI₃₀/ΔG₃₀ and AUCI had independent positive correlation with 25-(OH)D₃ (t values were 2.21 and 4.67, all P<0.01).

25-(OH)D₃ is lower in newly diagnosed T2DM, and associated with severity of blood glucose disorders. The shortage of vitamin D in T2DM may be correlated with decreased early-phase insulin secretion and whole insulin secretion.

To analyze the effect of microalbuminuria on predicting cardiovascular disease mortality and total mortality risk in 2181 subjects.

These subjects came from Beijing epidemiological data in the moderate-elderly population in June 2004. After 4 years follow up, the death of various reasons were observed of death of four-year period for various reasons in May 2008. In according to the albumin creatinine ratio(ACR) value, all subjects were divided into normal albuminuria group (NAU group), microalbuminuria group (MIAU group) and macroalbuminuria group (MAAU in according to the ACR). The various causes of death were analyzed, and the baseline clinical characteristics and metabolic markers were compared between the death group and survival group. In the follow-up, Cox regression model was used. After adjusted for age, DM history, history of hypertension, dyslipidemia and other potential risk factors, the relationship between ACR levels and cardiovascular- or all-cause mortality was analyzed.

Totally 77 subjects died during the 4 years follow up. The all-cause mortality was 8.7/1000 person-year in total population. The CVD and malignant tumor were the main causes of death. Compared with the survival population, the proportion of MIAU, MAAU, and DM were significantly higher in the death population(18.2% vs 8.7%, 9.1% vs 1.6%, 50.6% vs 25.8%, P<0.01). The all-cause mortality was 6.8‰, 20.6‰ and 58.8 ‰ in NAU, MIAU, MAAU population respectively. In the NAU population, malignant tumor was the leading cause of death, followed by cardiovascular disease. While in MIAU and MAAU population, cardiovascular disease was the primary cause of death. After age, blood glucose, hypertension, dyslipidemia and other factors were adjusted, compared with the NAU, the risk of death of cardiovascular disease was increased by 1.72 times and the all-cause death increased by 1.01 times in MIAU group, risk of death of cardiovascular disease increased by 3.87 times and of all-cause death increased by 2.76 times in MAAU group. NAU, as the control group, when adjusted for age, blood glucose, blood pressure, lipid disorders by Cox regression, 18.32% of CVD deaths and 11.96% of all deaths could be attributed to the ACR≥30 mg/g.

Cardiovascular disease and malignant tumor are the main mortality causes for the total population. In the NAU population, malignant tumor is the leading cause of death, followed by cardiovascular disease. In MIAU and MAAU population, cardiovascular disease is the primary cause of death. Compared with NAU group, CVD deaths and all-cause deaths are significantly increased.

To investigate the effect of urokinase-type plasminogen activator (uPA) on urokinase-type plasminogen activator (uPAR), plasminogen activator inhibitor-1 (PAI-1) and collagen type Ⅳ expression in the kidney of diabetic rats.

Twenty healthy male Sprague-Dawley rats (150 to 200 g) underwent intraperitoneal streptozotocin injection before being treated with or without 2500 U·kg^-1·d^-1 uPA for 4 weeks. Another 10 normal SD rats were used as controls. The rats were sacrificed at 29 days. Blood glucose and serum creatinine were measured. The kidney tissues were harvested to evaluate glomerular area, glomerular volume and mesangial area by using PASM dyeing. Expressions of uPAR, PAI-1 and collagen type Ⅳ were evaluated by immunohistochemistry. Analysis of variance and q test were used for data comparison.

Compared with the control group, DM group showed albuminuria ((25.4±4.3)mg/24 h vs (5.5±2.1) mg/24 h)and increased glomerular volume, mesangial area and expressions of uPAR, PAI-1 and collagen type Ⅳ. Intraperitoneal injection of uPA decreased the expressions of PAI-1 and type Ⅳ collagen in both kidney tissues and mesangial, although there was no significant difference in uPAR expression.

uPA may decrease the expression of PAI-1 instead of uPAR, which suggests that uPA might regulate the mesangial cells and its matrix expression through binding uPAR, uptaking PAI-1 and accelerating its degradation.

To investigate the effects of ribosomal protein S6 kinase 1 (S6K1) gene silencing on the pathogenesis of non-alcoholic fatty liver disease.

Twelve 9-week male db/db mice (body weight 44.5 to 48.2 g)were randomly assigned to the normal control group(n=6) and the study group(n=6). The mice in the study group were injected with S6K1 short hairpin RNA recombinant adenovirus (S6K1Ax) via the tail vein, and the control group was given U6 promoter recombinant adenovirus (pU6Ax). Six days after virus injection, db/db mice were killed and livers were harvested. Hepatic protein expression of insulin receptor substrate 1(IRS1), insulin receptor substrate 2(IRS2) and protein kinease B(Akt), Akt473 was determined by Western blot in the two groups. Total hepatic RNAs were extracted to analyze genes expression of fatty acids synthesis by using real-time quantitative reverse transcription polymerase chain reaction. Blood was collected after 16 h of fasting before db/db mice were killed. The serum free fatty acids, triglyceride and cholesterol levels were quantified by colorimetry. The data of the two groups were compared with t-test.

Six days after virus injection, fat droplet in hepatocyte decreased in study group compared with that in control group under HE staining observation and the fatty liver in study group was improved. Protein expression of S6K1 in the study group was down-regulated significantly compared with that in control group (0.12±0.01 vs 0.87±0.06, t=5.36, P<0.05); and the expression of IRS1, IRS2 and Akt473 were up-regulated in the study group than those in the control group (allP<0.05). Compared with those in control group, fatty acid synthesis genes of sterol regulatory element binding protein 1c (SREBP1c, 2.33±0.29 vs 1.34±0.39,t=3.46, P<0.01), fatty acid synthesis (7.8±1.2 vs 3.4±0.4,t=4.67, P<0.01), stearoyl-CoA desaturase 1 (SCD1, 764±116 vs 535±54,t=6.12, P<0.01) mRNA expression descended in the study group. Fasting blood FFA and cholesterol decreased in the study group compared with those in the normal group (t=2.64, P<0.05;t=4.25, P<0.01). No significant difference in serum triglycerol was detected between the two groups (P>0.05).

Given excess nutrient, over-activated hepatic ribosomal protein S6 kinase 1 maybe cause hepatic insulin resistance and fatty liver through negative feedback and up-regulating SREBP1c expression.

To investigate the effect of the glycine to serine mutations in codon 482 (Gly482Ser)gene polymorphism of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) gene on the transcription of gluconeogenesis key gene phosphoenolpyruvate carboxykinase (PEPCK).

(1) We designed to construct PGC-1α G1444A polymorphism expression plasmid using oligonucleotide based site directed mutagenesis and polymerase chain reaction and PEPCK promoter gene luciferase reporter plasmid PGL3-hPCK-luc using common PCR and restrictive enzyme digestion method first. And then wild-type plasmid with glycine in codon 482 pcDNA3.1-PGC-1α (G) and mutated plasmid with serine in codon 482 pcDNA3.1-PGC-1α (S) were co-transfected respectively with transcription factor expression plasmid pcDNA3.0-HNF4α into cultured HepG2 cell and L02 cell. (2) The mRNA and protein levels of PEPCK were detected after transfection 48 hours. Then PGL3-hPCK-luc and the reference plasmid PRL-SV40 were co-transfected according to different combinations. After 48 hours of culture the relative activity of luciferase was detected by the dual luciferase assay kit.One way ANOVA andt-test of independent samples were used for data analysis.

PGC-1α G1444A mutation plasmid and recombinant PGL3-hPCK-luc reporter plasmid were constructed successfuly. After being transiently transfected into liver cells, both the mRNA and protein levels of PGC-1α (G) and PGC-1α (S) were increased significantly, but there was no statistical significant difference between the two groups(P>0.05). The PEPCK mRNA and protein levels were increased significantly in both co-transfecting PGC-1α and HNF4α group(10.4±0.7 and 4.5±0.5) when compared with the sigle-transfection(0.86±0.18 and 0.99±0.09, bothP<0.05). Compared with PGC-1α (S) plus HNF4α group, the PEPCK mRNA and protein levels of PGC-1α (G) plus HNF4α group increased 1.83-fold(10.4±0.7 vs 5.35±0.23) and 1.4-fold(4.5±0.5 vs 3.0±0.4) in PGC-1α(G) plus HNF4α group (bothP<0.05). Moreover, Co-transfected PGC-1α plus HNF4α group had a significant promotion of PEPCK promoter activity compared with the single transfection PGL3-hPCK-luc group(28±5 vs 2.4±0.4,F=23.41, P<0.05); PEPCK promoter activity was increased 2-fold(83±10 vs 41±5,F=23.41, P<0.001)while being transfected with PGC-1α (G) into HepG2 cells than with PGC-1α (S). When transfected into L02 it was increased 2.25-fold(28±5 vs 13.0±1.5,F=60.75, P<0.001).

PGC-1α can coactivate hepatocyte nuclear factor 4α in promoting the transcription of PEPCK, while PGC-1α gene Gly482 has a more significant promotion by the activation of HNF4α than Ser 482. Accordingly, it is possible that the gene polymorphism can express protein with different structures, which would affect the protein-protein interactions.

Diabetes mellitus is a group of clinical syndromes with disorder of glucose metabolism as the main manifestation. Type 2 diabetes is mainly caused by insulin resistance and insufficient insulin secretion. With the increasing prevalence of obesity, high-calorie diet, and insufficient physical activity, the prevalence of type 2 diabetes is increasing year by year^[1]。 At present, although diabetes drug treatment is becoming more and more mature, it still can't achieve radical cure effect. Many diabetic patients need lifelong drug treatment, and with the progression of diabetes, pancreatic β cells are progressively destroyed, and many patients eventually need insulin. In recent years, it has been found that bariatric surgery has a significant and lasting effect on the control of hyperglycemia in patients with type 2 diabetes, and more and more clinical studies support this view.

Type 2 diabetes is often accompanied by increased incidence of cardiovascular events and mortality, which is a major problem faced by diabetic patients. Therefore, prevention and treatment of cardiovascular events is one of the main objectives of the treatment of type 2 diabetes.

According to the National Diabetes Epidemiological Survey organized by the Diabetes Branch of the Chinese Medical Association in 2007-2008, the prevalence of diabetes among adults over 20 years old in China is about 9.7%, and it is estimated that there are about 92.4 million adults with diabetes in China^[1]。 At the same time, the blood sugar control of diabetic patients in China is not optimistic. According to a survey conducted in 2006 on the management of patients with type 2 diabetes in China, the average glycosylated hemoglobin (HbA1c) of outpatients with type 2 diabetes in large and medium-sized cities surveyed was 7.6%±1.6%, and only 41.1% of patients achieved blood glucose control standard (HbA1c<7%)^[2]。 Insulin therapy is an effective hypoglycemic measure, but even if insulin therapy has been initiated, the blood sugar control situation is not satisfactory. According to the latest data from my country's glycation monitoring network, the overall blood sugar control of diabetic patients treated with oral hypoglycemic drugs combined with insulin is not ideal, with an average HbA1c of 8.38%; With the progression of diabetes mellitus, the function of pancreatic islet β cells continues to decline. In the course of insulin therapy, insulin therapy should be started as early as possible and adjusted in time to make the blood glucose of patients reach the standard, so as to reduce the impact of acute and chronic complications of diabetes mellitus on the life and quality of life of patients and the heavy economic burden caused by this^[3,4]。 In order to further standardize the national diabetes prevention and treatment work, in 2010, the Diabetes Branch of Chinese Medical Association organized national experts to revise the guidelines for the prevention and treatment of type 2 diabetes in China based on a large amount of evidence-based medical evidence. This revision also made some modifications in insulin intensive therapy.

A 76-year-old male was admitted to the hospital on 22 February 2011 due to "discovery of elevated blood sugar for 20 years and subcutaneous nodules after insulin injection for 10 months". The patient was found to have high blood sugar during physical examination 20 years ago, and was diagnosed as "diabetes" by oral glucose tolerance test. At that time, he had no obvious symptoms such as dry mouth, polydipsia and polyuria. After controlling his diet and exercise for more than one year, he started oral treatment with acarbose and metformin due to poor blood sugar control, and his blood sugar control was satisfactory. Microproteinuria was found in physical examination in 2009, and insulin therapy was recommended by an outside hospital. Since September 2009, low protamin zinc insulin (Novolin) 9U was injected subcutaneously before bedtime. There was no obvious discomfort in the initial stage of treatment, and the insulin dose was gradually increased. On April 16, 2010, the patient developed a wheal at the injection site several minutes after 14 U of low-protamine zinc insulin before bed, accompanied by pruritus, and gradually merged into tablets. There were no symptoms such as dyspnea or dizziness. The rash subsided in the morning on the second day after oral administration of cetirizine 10 mg, and Novolin N was discontinued thereafter. In July 2010, the patient was admitted to our hospital. The total serum IgE was 211 kU/L (normal reference value ≤60 kU/L). The insulin-specific IgE of bovine, pig and human was grade 2, and the protamine-specific IgE was grade 0. The diagnosis was "insulin allergy". Recombinant human insulin (Novolin R, N, 30R, 50R and Humulin R, N, 70/30), 0.1 ml of normal insulin (containing 1 U of insulin) and 0.1 ml of normal saline (negative control) were injected intradermally, and short-acting human insulin (Novolin R) with the least allergic reaction in skin test was selected for insulin desensitization treatment. Starting from subcutaneous injection at 0.005 U, the dose was gradually increased, and obvious wheal (3 mm in diameter) with itching appeared at 3 U, and the desensitization treatment was stopped at that time. Switched to oral repaglinide 2 mg and acarbose 100 mg, both 3 times/d, and discharged after optimal glycemic control.

The 2011 China Forum on Diabetic Foot and Related Diseases was held in Hangzhou from May 27 to 29, 2011. The conference was sponsored by the Diabetes Branch of Chinese Medical Association, hosted by the Diabetes Branch and the Peripheral Vascular Disease Group, and co-organized by the 306th Hospital of the People's Liberation Army, Friends of Diabetes magazine and the Second Affiliated Hospital of Zhejiang University. The conference invited a number of well-known experts from home and abroad to give special presentations. Nearly 700 doctors and nurses from all over the country, including Hong Kong, attended the congress.

The purpose of this study was to clarify the presence of insulin resistance in patients with type 1 diabetes and the role of insulin in adipose tissue, and to evaluate whether its efficacy is related to the effect of glycemic control, body mass index, disease course, and glycosylated hemoglobin level.

This study aimed to evaluate the efficacy and safety of metformin and thiazolidinediones, including pioglitazone and rosiglitazone, in the treatment of polycystic ovary syndrome through a meta-analysis.

The incidence and mortality of coronary heart disease are higher in diabetic patients. In the treatment guidelines, reducing LDL cholesterol is the primary treatment goal, and reducing non-HDL cholesterol and apolipoprotein B is the secondary treatment goal.

The main characteristic of type 2 diabetes is the loss of islet beta cell function and total volume, and the recently proposed endoplasmic reticulum stress may be an important cause of this. The purpose of this study was to investigate the protective effect of glucagon-like peptide-1 receptor agonists on endoplasmic reticulum stress-mediated beta cell apoptosis.

For patients with diabetes, impaired fasting blood glucose, and abnormal glucose tolerance, the ideal blood pressure control target is not yet determined.

Studies have shown that the autoimmune response of human islet beta cells is often accompanied by abnormal adipose tissue metabolism. This study aimed to investigate the correlation between C-peptide concentration and free fatty acids in pediatric patients with type 1 diabetes.

The main pathogenesis of diabetic retinopathy is the increase of neovascularization and vascular permeability caused by overexpression of vascular endothelial growth factor. This study focused on miRNA-200b and its downstream target factor, vascular endothelial growth factor, to explore the role of miRNA alterations in the pathogenesis of diabetic retinopathy.

Type 2 diabetes is a common cause of secondary osteoporosis. The researchers designed a cross-sectional survey to study the association of diabetes with fragile vertebral fractures in men with acromegaly.

Gastric bypass can significantly reduce the body weight of patients. In obese patients with type 2 diabetes, gastric bypass results in better glycemic control than patients with equal weight loss after simple dietary control, and its metabolic mechanism is currently unclear.

It is generally believed that hyperfree fatty acidemia mediates insulin resistance in obese people. Previous studies have shown that gastric bypass improves the effect of insulin on glucose metabolism. However, the effect of gastric bypass on adipose tissue insulin sensitivity in non-diabetic patients is unknown. It has been speculated that gastric bypass treatment can increase insulin sensitivity, but it is still lower than that of thin people.

The overall quality of lower extremity revascularization studies on diabetic foot ulcer with peripheral arterial lesions is low and significantly biased. The study showed that the mortality rate of perioperative period was generally low, but the major systemic complications of perioperative period were obvious, about 10%. There seemed to be no significant difference between open surgery and endovascular technique in mortality and complication rate. The mortality rate is high after long-term follow-up after surgery, so patients with diabetes combined with ischemic foot ulcer need to receive more aggressive and appropriate medical treatment targeting risk factors to reduce long-term mortality rate. Current data show that revascularization should often be considered for patients with diabetic foot ulcer complicated with ischemia, but it is not clear whether it has an additional effect on patients with mild blood perfusion abnormalities. End-stage renal disease is one of the major risk factors for foot ulcers and amputations in diabetic patients. These patients are often difficult to treat and have a high long-term mortality rate. There are no randomized controlled studies directly comparing the role of open surgery and endovascular revascularization in diabetic patients with ischemic ulcer. Therefore, there is insufficient information to demonstrate which is more effective, open surgery or endovascular intervention. Therefore, it is indeed necessary to standardize the reporting of patient baseline demographic data, disease severity and prognosis. These criteria should consider both the characteristics of the patient's peripheral arterial disease and wound.

Evidence for high-quality therapeutic interventions in diabetic foot infections is very limited. Evidence in support of early surgical intervention is based on two studies with high risk bias. The study of colony-stimulating factor CSF is of high quality but the results are contradictory. Only one of all randomized controlled trials comparing antibiotic treatment regimens reported differences in infection-related outcomes. The clinical and microbiological efficacy of the topical antibiotic persiganam was not inferior to that of the oral broad-spectrum antibiotics quinolone and ofloxacin. Persiganam has fewer side effects than ofloxacin. However, the long-term side effects of this topical medication are unknown. Data on skin and soft tissue infections confirm early observations that Gram-positive bacteria play an important role in diabetic foot infection. Nonetheless, there is growing observational evidence that Gram-negative bacteria are of greater significance in populations outside the Western Hemisphere and South Asia. It is worth mentioning that no large differences were observed between the relatively broad or narrow spectrum treatment regimens. The best antibiotic choice, route of administration, and course of treatment still need to be supported by studies with sufficient evidence. Available data do suggest that oral antibiotics may be used in outpatient clinics to treat certain diabetic foot infections.