Volume 14 · Issue 05 · 2022

Diabetes mellitus is characterized by elevated blood glucose, which is influenced by many factors in the internal and external environment. Its clinical manifestations and pathophysiological changes are multidimensional and highly heterogeneous. Rooted in the established "blood sugar-centric" thinking, it has been different from the diagnosis and treatment needs of type 2 diabetes reflected by evidence-based medical evidence in recent years. Understanding the pathophysiological mechanism of type 2 diabetes is analogous to the implementation of the "black box method" in cybernetics, but there are still many outstanding problems that need to be solved before clarifying the "black box" and realizing accurate model prediction.

It has long been believed that intensive hypoglycemia can only ameliorate microvascular complications of diabetes, but not alter cardiovascular outcomes in diabetic patients. Therefore, both domestic and foreign guidelines use glycated hemoglobin (HbA_1c) Meet the standard to formulate the path of diabetes drug treatment. Studies have shown that sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists have the effect of significantly improving cardiorenal outcomes in diabetic patients. The concept of diabetes treatment has undergone a fundamental change, that is, the treatment pathway aimed at controlling blood glucose has changed to the treatment strategy aimed at improving cardiorenal outcomes. Based on the changes of diabetes prevention and treatment guidelines at home and abroad, this paper expounds the constantly updated diabetes treatment concept and the evidence-based medical evidence behind it.

Adolescent-onset adult diabetes mellitus (MODY) is a special type of diabetes mellitus. So far, 14 types of MODY have been reported, accounting for about 1% to 5% of diabetic patients. The onset of MODY is often insidious and often missed clinically. With the deepening of the understanding of the clinical characteristics of MODY and the rapid development of molecular biology detection technology, more and more patients with MODY are detected and diagnosed early. This consensus aims to help patients with MODY in early detection, correct diagnosis and precise treatment, and promote standardized screening, diagnosis and treatment of MODY.

To investigate the use of statins in patients with type 2 diabetes (T2DM) in Beijing.

A non-interventional observational study of inpatients and outpatients with T2DM in a total of 6 hospitals from August 2015 to March 2016. According to the questionnaire, the patients were divided into the current statin use group, the previous statin use group and the statin non-use group. Variance analysis or t test analysis was used to compare the use of statins and the compliance rate of blood lipids among diabetic patients in each group, and logistic regression analysis was used to evaluate the influencing factors of discontinuation of statins.

A total of 1 518 patients with T2DM were included in the study, of which 45.9% (696/1 518) were current statin users, 10.9% (166/1 518) were former statin users, and 43.2% (656/1 518) were non-users of statins. The compliance rates of total cholesterol (TC), total low-density lipoprotein cholesterol (LDL-C) and total triglyceride (TG) were 52.0% (789/1 518), 54.0% (820/1 518) and 60.7% (922/1 518), respectively. The blood lipid compliance rate of diabetic patients ≥65 years old (639 cases) was higher than patients younger than 65 years old (879 cases);current statin users had higher TC and LDL-C compliance rates than former statin users and statin non-users (both P<0.001).The reasons why patients stopped using statins were as follows: 33.1% (79/239) of people believed that their blood lipids were well controlled; 29.3% (70/239) were afraid of side effects of drugs; 18.4% (44/239) had side effects after taking the drugs. According to logistic regression analysis, age ≥ 65 years (OR=1.847, 95%CI 1.088-3.134, P=0.023), diabetic course ≥ 10 years (OR=2.752, 95%CI 1.369-5.531, P=0.039), poor understanding of diabetes (OR=3.209, 95%CI 1.393-7.393, P=0.006) and LDL-C target intervals (OR=4.111, 95%CI 1.364-12.390, P=0.012) were related with discontinuation of statins.

The success rate of blood lipids of current users of statins is higher than that of previous users and non-users of statins. The use of statins in patients with T2DM in Beijing is still significantly insufficient.

To systematically evaluate the prevalence and influencing factors of eating behavior disorder (DEB) in adolescents with type 1 diabetes mellitus (T1DM).

Ten Chinese and English databases including PubMed, Cochrane Library, EMBase, Journal of American Medical Association (JAMA), Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycINFO, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Database, Wanfang database and VIP were retrieved. The literatures evaluating DEB prevalence and influencing factors of T1DM adolescents were included. The retrieval time was from the database construction to November 2021. Two researchers independently screened the literatures, extracted the data and evaluated the risk of bias in the included studies. The prevalence of comorbidities was analyzed by Stata 14.0 software and descriptive analysis was performed on the influencing factors.

A total of 16 literatures were included, including 4 652 T1DM adolescents, published between 2010 and 2021. Meta analysis showed that DEB prevalence rate of T1DM adolescents was 34% (95%CI 25%—46%). DEB prevalence was higher in female (51%, 95%CI 38%—69%), Asian (45%, 95%CI 22%—89%) and published between 2015 and 2018 (45%, 95%CI 21%—96%). Descriptive analysis showed that the influencing factors of DEB in T1DM adolescents included internal factors (female, body dissatisfaction, etc.), psychosocial factors (depression, low self-esteem, etc.) and family factors (low educational level of parents).

The prevalence of DEB in T1DM adolescents is high. Female, body dissatisfaction, depression, low self-esteem and low educational level of parents can increase the risk of DEB in T1DM adolescents.

To integrate data to clarify the prevalence of sarcopenia and its influencing factors in diabetic patients using Meta-analysis.

Pubmed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), Wanfang, China Biomedical Literature (CBM) and VIP databases were retrieved from the establishment of the database to November 30, 2020 for all relevant literature on the prevalence of sarcopenia in diabetic patients. Sample size, gender of subjects, study area and study environment, prevalence of sarcopenia, 95%CI and influencing factors were extracted from the included literature. The prevalence of diabetic sarcopenia was analyzed by random effect model and the influencing factors of diabetic sarcopenia were analyzed by subgroup.

A total of 45 studies involving 12 379 individuals were included. The pooled prevalence of sarcopenia in diabetic patients was 18.0% (95%CI 16.0%-20.0%). Subgroup analysis showed that the prevalence of sarcopenia was 19.0% (95%CI 17.0%-22.0%) in males and 17.0% (95%CI 15.0%-20.0%) in females. The prevalence of sarcopenia was 19% (95%CI 17.0%-21.0%) in Asia, 13.0% (95%CI 8.0%-18.0%) in South America, and 9.0% (95%CI 0-17.0%) in Oceania. The prevalence of sarcopenia was 18.0% (95%CI 16.0%-20.0%) in hospitalized patients and 15.0% (95%CI 4.0%-26.0%) in community patients.

The total prevalence of sarcopenia in diabetic patients was 18.0%. Male, Asian and hospitalized diabetic patients might be more prone to sarcopenia.

To explore the application of novel urinary metabolite biomarkers in diagnosis of diabetic kidney disease (DKD).

A total of 235 healthy individuals and type 2 diabetes mellitus (T2DM) patients admitted to the Second Affiliated Hospital of Nanjing Medical University from January to December 2020 were enrolled in this cross-sectional study. Two separated discovery cohort (116 cases) and validation cohort (119 cases) were included: the discovery cohort was divided into healthy control group (37 cases), simple T2DM group (40 cases) and T2DM combined with DKD group (39 cases), and the validation cohort was divided into simple T2DM group (64 cases) and T2DM combined with DKD group (55 cases). Demographic and laboratory data were collected, and the urinary metabolites were detected by ultraperformance liquid chromatography coupled to tandem mass spectrometry. Partial least squares discriminant analysis and orthogonal partial least squares discriminant analysis were used for multi-dimensional modeling. Machine learning based on Boruta algorithm was used to screen potential markers. Wilcoxon test was used for comparison of novel urinary metabolite biomarkers data between two groups, and Kruskal-Wallis test was used for comparison between multiple groups. Binary logistic regression analysis was used for statistical modeling, and receiver operating characteristic (ROC) curve was used to evaluate diagnostic efficacy.

In discovery cohort, a total of 160 metabolites were detected in morning urine samples by targeted quantitative metabolomics, 62 differential metabolites were screened out from the discovery cohort, mainly enriched in amino acid metabolic pathway, and 17 of which were candidate markers for diagnosis of DKD. Fifteen differential metabolites and seven candidate markers (isovaleric acid, isobutyric acid, leucine, s-adenosylhomocysteine, propionic acid, oxoadipic acid, propionylcarnitine) were verified in the validation cohort. The diagnostic model of the combined marker was constructed by integrating the 7-candidate urinary metabolic markers. The diagnostic efficacy of the combined marker in both the discovery cohort and the validation cohort (the area under ROC curve of the discovery cohort was 0.888, 95%CI 0.814-0.963; the area under ROC curve of the validation cohort was 0.811, 95%CI 0.734-0.887) were significantly higher than that of a single metabolic marker (the area under ROC curve of the discovery cohort was 0.697-0.831, the area under ROC curve of the validation cohort was 0.628-0.728).

There were significant differences in urine metabolites between simple T2DM patients and T2DM combined with DKD patients. The combination of various urine metabolic markers might be a novel strategy to diagnose DKD.

To investigate the effect of nicorandil on myocardial ischemia-reperfusion injury in rats with type 2 diabetes mellitus (T2DM).

A total of 60 SD rats were randomly divided into 6 groups: non-diabetic sham (Sham) group, non-diabetic ischemia-reperfusion (I/R) group, non-diabetic nicorandil-ischemia-reperfusion (Nic) group, diabetic sham (DM Sham) group, diabetic ischemia-reperfusion (DM I/R) group, diabetic nicorandil-ischemia-reperfusion (DM Nic) group (10 animals in each group). T2DM rat model was established by injecting low-dose streptozotocin plus high fat and high sugar diet, and then myocardial ischemia reperfusion model was established in the circumstance. At the end of reperfusion, serum was obtained to determine creatine kinase isoenzyme (CK-MB), nitric oxide (NO) level, myocardial tissue reactive oxygen species (ROS) content, myocardial infarct area. Moreover, in the heart tissue sections, the hematoxylin-eosin (HE) staining, terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining and wheat germ agglutinin (WGA) staining were performed respectively. The myocardial tissue protein kinase B (Akt), phosphorylated glycogen synthase kinase 3β (GSK3β) and endothelial nitric oxide synthase (eNOS) protein phosphorylation levels were measured by western blotting. The experimental data were compared between multiple groups using one-way analysis of variance (ANOVA), and the Dunnett′s test was used for two-way comparison between groups.

Compared with rats in I/R group, myocardial infarct area, degree of myocardial tissue damage and myocardial apoptosis rate in DM I/R group were more severe (P<0.01). Serum CK-MB (P<0.01) and myocardial tissue ROS content (P<0.01) were significantly lower, serum NO level (P<0.01) was significantly higher, and the myocardial infarct area (P<0.01) and myocardial apoptosis rate (P<0.01) were significantly lower in DM Nic group than in DM I/R group. Myocardial infarct area (P<0.01) and myocardial apoptosis rate (P<0.01) were significantly reduced, and the phosphorylation levels of Akt, GSK3β and eNOS protein (P<0.05) were significantly increased. However, the myocardial infarct area (P<0.01), apoptosis rate (P<0.01), CK-MB in serum (P<0.01) and ROS in myocardial tissues (P<0.01) were still higher in DM Nic group than in Nic group, and the phosphorylation levels of Akt, GSK3β and eNOS (P<0.01) were also lower than those in Nic group. However, there was no statistically significant difference in the serum levels of NO between DM Nic group and Nic group (P>0.05).

Nicorandil might reduce myocardial ischemia-reperfusion injury in T2DM rats by activating the Akt signaling pathway.

To investigate the mechanism of long noncoding RNA potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (Kcnq1ot1) affecting insulin secretion of pancreatic β cells by regulating miR-92a-1-5p.

From June to December 2020, 25 patients with newly diagnosed type 2 diabetes mellitus (T2DM) were recruited in the Third Affiliated Hospital of Sun Yat-sen University, and 21 age-matched subjects without diabetes were recruited as a control group. Age, body mass index (BMI), fasting plasma glucose (FPG) and glycated hemoglobin A_1c (HbA_1c) were collected, and the expression of Kcnq1ot1 in serum was detected by quantitative real-time PCR (qRT-PCR), and its correlation with FPG and HbA_1c was analyzed. 5-week-old male C57BL/6J mice were randomly divided into high-fat diet (HFD) group (n=6) and chow diet (CD) group (n=6). After 20 weeks of feeding, the RNA of primary pancreatic islet cells was extracted. MIN6 cells cultured in vitro were divided into bovine serum albumin (BSA) group and palmitic acid (PA, 400 μmol/L) group. According to whether Kcnq1ot1 siRNA was transfected or not, the cells were divided into si-NC group and si-Kcnq1ot1 group. According to whether miR-92a-1-5p mimics or inhibitors were transfected or not, the cells were divided into mimic control group, mimics group, inhibitor control group and inhibitors group. According to whether the inhibitors was added after transfection of Kcnq1ot1/NC siRNA, the cells were divided into si-NC+inhibitor control group, si-Kcnq1ot1+inhibitor control group, si-NC+inhibitors group, si-Kcnq1ot1+inhibitors group. qRT-PCR was used to detect the expression level of Kcnq1ot1, miR-92a-1-5p, insulin transcript 1 (Ins1), insulin transcript 2 (Ins2), insulin receptor (Insr), NK6 homeobox protein 1 (Nkx6.1), insulin receptor substrate 1 (Irs1) and neurogenin 3 (Ngn3). Western blotting was used to detect the expression level of insulin and Insr. Glucose stimulated insulin secretion assay was used to detect the level of insulin. Double luciferase reporting gene assay was used to verify the direct relationship between Kcnq1ot1 and miR-92a-1-5p. Statistical analysis was performed using independent samples t test, analysis of variance, and Pearson correlation analysis.

The expression of Kcnq1ot1 in the serum of patients with type 2 diabetes was significantly lower than that of the control group (P<0.01), and the expression of Kcnq1ot1 was negatively correlated with FPG and HbA_1c. Compared with CD group, the expression of Kcnq1ot1 in islets of HFD group was down-regulated (P<0.001). In MIN6 cells, compared with BSA group, the expression of Kcnq1ot1 in PA group was down-regulated (P<0.01). Compared with the si-NC group, the GSIS in the si-Kcnq1ot1 group was decreased (P<0.05), and the mRNA levels of Ins1, Ins2, Insr, Nkx6.1, Irs1 and Ngn3, and the protein levels of Insr and insulin were all decreased in the si-Kcnq1ot1 group (P<0.05). Compared with the mimic control group, the GSIS in the mimics group was decreased (P<0.05), and the mRNA levels of Ins1, Ins2, Insr, Nkx6.1, Irs1 and Ngn3, and the levels of Insr and insulin were reduced (P<0.05). Compared with the inhibitor control group, the GSIS in the inhibitors group was increased (P<0.05), and the mRNA levels of Ins1, Ins2, Insr, Nkx6.1, Irs1 and Ngn3 were increased in the inhibitors group (P<0.05). The protein levels of Insr and insulin were increased (P<0.05). Double luciferase reporting gene assay showed that the luciferase activity decreased after co-transfection with the mimics and Kcnq1ot-WT plasmid (P<0.05), and after co-transfection with inhibitors and Kcnq1ot1-WT plasmid, the luciferase activity was significantly increased (P<0.05). Compared with si-NC group, the expression of miR-92a-1-5p in si-Kcnq1ot1 group was increased (P<0.05). Compared with si-Kcnq1ot1+inhibitor control group, the transcript levels of Ins1, Ins2, Insr, Irs1 and Ngn3 and the protein levels of insulin and Insr in MIN6 cells in si-Kcnq1ot1+inhibitors group were increased (P<0.05).

Long noncoding RNA Kcnq1ot1 might affect the function of pancreatic β-cells by targeting miR-92a-1-5p.

To investigate the effect and mechanism of mitofusin 2 (Mfn2) on palmitic acid (PA)-treated mouse pancreatic β cells.

Mouse pancreatic β-cell MIN6 cells were treated with PA in a concentration gradient, and cell viability was detected by CCK8 method, and the PA concentration in subsequent experiments was determined. Mfn2 knockdown and Mfn2 overexpression stable cell lines were constructed by lentivirus transfection using MIN6 cells. Each group was named as Mfn2 knockdown empty-load control (ShNC-Mfn2) group, Mfn2 knockdown (Sh-Mfn2) group, Mfn2 overexpression empty-load control (OENC-Mfn2) group, Mfn2 overexpression (OE-Mfn2) group, ShNC-Mfn2+PA group, Sh-Mfn2+PA group, OENC-Mfn2+PA group, and OE-Mfn2+PA group. Cells were treated with bovine serum albumin as PA control and PA. Flow cytometry was used to detect the apoptosis rate, intracellular reactive oxygen species (ROS) level and mitochondria membrane potential level in each group. Microplate reader was used to detect the intracellular ATP level. Real-time fluorescence quantitative polymerase chain reaction and Western blotting were used to detect Mfn2 and apoptosis-related protein [Caspase-3, B cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax)] mRNA and protein expression. The t-test was used for comparison between two groups, and the one-way analysis of variance (ANOVA) was used for comparison between multiple groups.

Compared with 0 mmol/L PA, the cell viability was significantly decreased when the PA concentrations were 0.125,0.250, 0.500, 0.750, and 1.000 mmol/L (P<0.01). The PA concentration with a cell viability of about 50% (0.5 mmol/L) was selected as the follow-up experiment. At this time, the cell survival rate was 43.53%±0.56%. After adding 0.5 mmol/L PA to MIN6 cells, the mRNA and protein expressions of Mfn2 were significantly decreased (P<0.01). Compared with the ShNC-Mfn2 group, the levels of mRNA and protein of Mfn2 in the Sh-Mfn2 group decreased (P<0.05); compared with the OENC-Mfn2 group, the mRNA and protein levels of Mfn2 in the OE-Mfn2 group increased (P<0.01). Compared with the ShNC-Mfn2+PA group, the ROS in the Sh-Mfn2+PA group was significantly increased (P<0.01), and the ATP and mitochondrial membrane potential levels were significantly decreased (P<0.05). Compared with the OE-Mfn2+PA group, the ROS level was decreased, and the ATP level and mitochondrial membrane potential were significantly higher (P<0.05). Compared with ShNC-Mfn2+PA group, the apoptosis rate of Sh-Mfn2+PA group was increased (P<0.01). Compared with OENC-Mfn2+PA group, the apoptosis rate of OE-Mfn2+PA group was decreased (P<0.01). Compared with the ShNC-Mfn2+PA group, the mRNA and protein levels of Bax and Caspase-3 in the Sh-Mfn2+PA group were significantly increased, and the mRNA and protein levels of Bcl-2 were significantly decreased (P<0.05). Compared with the OENC-Mfn2+PA group, the mRNA and protein levels of Bax and Caspase-3 in the OE-Mfn2+PA group were significantly decreased, and the mRNA and protein levels of Bcl-2 were significantly increased (P<0.05).

Mfn2 could ameliorate the PA-induced lipotoxicity of MIN6 cells, and overexpression of Mfn2 had a protective effect on MIN6 cells under lipotoxicity, in addition, knockdown of Mfn2 aggravated the lipotoxicity of MIN6 cells.

To explore whether palmitic acid (PA) can induce ferroptosis in pancreatic beta-cell line MIN6 cells.

Pancreatic beta-cell line MIN6 cells were divided into normal group, PA group (1.0 mmol/L), PA+apoptosis inhibitor (Z-VAD-FMK) group (5 μmol/L), PA+ ferrostain-1(Fer-1) group (5 μmol/L), PA+ necrostatin-1(Nec-1) group (5 μmol/L). Each group was set three parallels. Cell viability was detected by CCK8 method. Cellular ultrastructure was assessed with electron microscopy. FerroOrange was used to detect intracellular Fe²⁺. The lipid peroxidation assay kit was used to detect the concentration of malondialdehyde (MDA). Flow cytometry was used to detect intracellular reactive oxygen species (ROS) levels. Real-time quantitative polymerase chain reaction was used to detect the mRNA levels of caspase3, receptor-interacting protein kinase 3 (RIPK3), acyl-CoA synthetase long-chain family member 4 (ACSL4), prostaglandin endoperoxidase synthase 2 (Ptgs2), arachidonate lipoxygenase 15 (ALOX15), ferritin heavy chain (FTH), ferritin light chain (FTL), and glutathione peroxidase 4 (GPX4). Western blotting was used to detect the proteins levels of cleaved caspase3, RIPK3, ACSL4, ALOX15 and Ptgs2. The t-test was used to compare two groups.

Compared with the PA group, cell viability of MIN6 was higher in PA+Z-VAD-FMK group, PA+Fer-1 group or PA+Nec-1 group (P<0.01). MIN6 cells, which were treated with PA to exhibit the characteristic morphologic features, were associated with apoptosis, necrosis and ferroptosis under electron microscope. Compared with the control group, in PA group, the levels of the cellular intracellular Fe²⁺, MDA and total lipid ROS were increased. The mRNA relative expression levels of caspase3, RIPK3, ACSL4, Ptgs2 and ALOX15 were increased. The mRNA relative expression levels of FTH and GPX4 were decreased. The protein relative expression levels of cleaved caspase3, RIPK3, ACSL4, ALOX15 and Ptgs2 were increased (all P<0.01). Compared with the PA group, in PA+Fer-1 group, the levels of cellular intracellular Fe²⁺, MDA and total lipid ROS were decreased. The mRNA relative expression levels of ACSL4, Ptgs2 and ALOX15 were decreased. The mRNA relative expression levels of FTH and GPX4 were increased. The protein relative expression levels of ACSL4, ALOX15 and Ptgs2 were decreased (all P<0.01).

PA could induce ferroptosis in pancreatic beta-cell line MIN6 cells.

The diagnosis and treatment of non-hyperglycemic diabetic ketoacidosis (euDKA) in an unrecognized patient with acromegaly complicated with diabetes was reported after treatment with sodium glucose cotransporter 2 inhibitor (SGLT2i). The patient went to the local hospital with "dry mouth, polydipsia and polyuria" as the first manifestation. After using SGLT2i hypoglycemic treatment, he experienced "nausea and vomiting for 1 day" and went to our hospital. The patient's blood glucose, blood ketone bodies, anion gap and lactic acid were all increased, the arterial blood gas analysis pH was 7.13, and the actual bicarbonate decreased, and the diagnosis was euDKA. SGLT2i was immediately discontinued, intravenous fluid rehydration and continuous insulin pumping was given. Growth hormone and insulin-like growth factor were both elevated, and magnetic resonance showed a huge occupation of the sellar region, which was diagnosed as acromegaly. Surgical resection by nasosphenoidal approach, histopathological examination revealed pituitary growth hormone adenoma. We compiled the diagnosis and treatment of this patient to warn clinicians that the use of SGLT2i in patients with active acromegaly and diabetes may cause euDKA, and use it cautiously to reduce the occurrence of drug-related adverse outcomes.

Diabetic scleredema (SD) is a serious type of scleredema and is a rare clinical connective tissue disease. The characteristic clinical manifestations of SD are local or diffuse non-depressed swelling, hardness and thickening of the skin, unclear boundary with surrounding tissues, unclear etiology and pathogenesis, easy to ignore in clinical work, difficult treatment and poor prognosis. A case of SD is reported and literature review is conducted, hoping to improve clinicians' understanding and diagnosis and treatment level of this disease through this case.

A new insulin receptor gene heterozygous mutation caused by type A insulin resistance syndrome (TAIRS) family was reported. The proband was admitted to the hospital with the main complaint of "irregular menstruation for 5 years". He had acanthosis nigricans, hyperandrogenemia and insulin resistance. The mother and brother in the family had hyperinsulinemia. Insulin receptors were detected in all 3 cases by whole exon gene sequencing (INSR) gene c.3163G>C (p.A1055P) heterozygous mutation, all diagnosed as TAIRS. The proband was treated with metformin, and the insulin level decreased significantly. This article discusses its clinical characteristics, diagnosis and treatment points in combination with the literature, aiming at improving the clinicalINSRRecognition of patients with TAIRS caused by genetic mutations.

Diabetic nephropathy (DKD) is a chronic kidney disease caused by diabetes. At present, China has become the country with the largest number of diabetic patients in the world, and the incidence of DKD is gradually increasing in recent years. DKD can cause kidney damage and may eventually progress to end-stage renal disease; It is also prone to multiple complications, increasing the risk of cardiovascular disease and death in patients. Timely diagnosis and effective management of DKD and delaying the disease progression are still major clinical challenges. Diagnosis and treatment modes such as early screening and life management, risk factor control and multi-disciplinary collaborative comprehensive management based on individualized principles are currently recognized scientific DKD management strategies. This article reviews the latest progress in the pathogenesis, screening and diagnosis, management and treatment of DKD, so as to deepen clinicians' understanding of DKD and provide reference for its clinical diagnosis and treatment.

Brown adipose tissue (BAT) is the main site of non-trembling thermogenesis in humans. Many studies have proved that transplanted BAT has important roles such as weight loss, improving glucose metabolism, and reversing type 1 diabetes. The mechanism of action includes activating endogenous BAT, promoting the expression of thermogenesis-related genes, increasing the body's energy consumption, and improving glucose and lipid metabolism and reducing adipose tissue inflammation through secretion of brown adipocytokines. The role of BAT in energy regulation and systemic metabolism provides new ideas for weight loss and improvement of abnormal glucose and lipid metabolism, and BAT transplantation has also become a possible way to treat obesity and related metabolic diseases.

Oral glucose tolerance test (OGTT) is a glucose stress test, which is mainly used to evaluate the body's ability to regulate blood glucose. In recent years, more and more attention has been paid to the relationship between blood glucose curve morphology and islet function of OGTT in different populations. The morphology of blood glucose curves mainly includes monophasic and biphasic blood glucose curves and blood glucose peak time. Among them, the monophasic blood glucose curve shape can be used as a predictor of islet dysfunction and diabetes risk in different populations. At the same time, with the delay of blood glucose peak time, individual islet function deteriorates, and the risk of developing diabetes in the future also increases. This article reviews the relationship between blood glucose profile morphology and individual islet function during OGTT.

It is a challenge for many researchers to improve the quality of clinical research and produce high-level and standardized clinical research results. The quality of clinical research restricts the overall level of clinical research, affects research innovation and transformation of achievements, and is the key to producing high-quality research. This paper analyzes the status quo of clinical research quality management from several aspects, including the objectives and principles of clinical research quality management, regulations and regulatory requirements, and the current main management mode. At the same time, focusing on the four aspects of project execution progress, execution quality, ethical compliance and scientificity, the paper sorts out the risk-based quality monitoring indicators, deeply discusses the common quality problems in current clinical research, and gives corresponding improvement suggestions, aiming at providing reference and reference for researchers to improve the quality of clinical research.