Volume 01 · Issue 02 · 2009

To investigate the effects of free fatty acids (FFAs) on gene expression of G protein coupled receptor 40 (GPR40) and the insulin secreting function in βTC–3 cell, and the intervening influence of pioglitazone (Piog) on FFA–induced these impairment of βTC–3 cell.

βTC–3 cells were cultured in vitro and divided into control group, FFAs group, Piog group and Piog+ FFAs group, then the mRNA of GPR40 was detected by nested semi–quantitative reverse transcription polymerase chain reaction (RT–PCR). The protein concentration was determined with BCA kit, and insulin secretion was examined in every group by radioimmunoassay. Data analysis was assessed by using one–way ANOVA and Bivariate Correlation.

(1)The cell morphology and gene expression of GPR40 were not varied in each level FFAs groups for 12 h, but the cells were transformed and gene expression of GPR40 was decreased with the prolongation of intervening duration in different groups (F_{24 h}=5.475, F_{48 h}=25.923, all P<0.05). (2)BIS and GSIS in βTC–3 cells were not changed after the treatment of FFAs in the range of 0.25 to 1.0 mmol/L for 12 h, but with the prolongation of duration (24 or 48 h), the cells which were exposed to FFAs showed a decreased in BIS and GSIS (F_{24 h BIS}=6.876, F_{48 h BIS}=12.421, F_{24 h GSIS}=27.767, F_{48 h GSIS}=36.382, all P<0.05). (3)When the cells were cultured with 1.0 mmol/L FFAs in the presence of 0.1 to 10 μmol/L Piog, a dose–dependent increase of gene expression of GPR40 and insulin secretion were induced in the co–treated groups (F_GPR40=14.303, F_INS=56.618, all P<0.05).

Elevated FFAs may inhibit the gene expression of GPR40, and impair insulin secretion function of βTC–3 cells. Piog may be able to resist this impairment of FFAs.

To investigate the impact of fasting plasma glucose level on duration of hospitalization, recurrence and mortality rate of acute cerebral infarction.

A retrospective study was conducted in 974 patients with acute cerebral infarction admitted during February 1996 and December 2006. Fasting plasma glucose, lipid profile, and blood pressure were measured. Time of hospital stay was recorded. Disease recurrence and complications were followed up. Multiple linear regression analysis, Logistic regression analysis, Chi–square test, and Kruskal–Wallis test were used for data analysis.

The recurrence, duration of hospitalization, and mortality rate of the patients with acute cerebral infarction were positively correlated with fasting plasma glucose level at admission. The mortality rate was increased to 50.00% when fasting plasma glucose≥11.1 mmol/L and low–density lipoprotein cholesterol≥3.5 mmol/L. The mortality rate was also increased to 33.33% or 30.00% in the participants with fasting plasma glucose≥11.1 mmol/L and diastolic blood pressure ≤80 mm Hg (1 mm Hg=0.133 kPa) or ≥100 mm Hg.

The fasting plasma glucose level may be strongly associated with during of hospitalization, disease recurrence, and mortality rate in patients with acute cerebral infarction. Plasma glucose monitoring and early intervention and treatment might be able to reduce the recurrence and mortality of cerebral infarction.

To identify the clinical spectrum and the clinical diagnostic criteria of laminopathy.

We here reported a novel laminopathy case. Based on the clinical features of the case and overall review on the related literatures, we aimed to identify the clinical characteristics including involved tissue origination, clinical diagnosis, differentiation diagnosis, treatment and prognosis of laminopathy. Multiple systems including skin, skeleton, skeletal muscle, cardiac muscle, nerve and adipose tissue were estimated by laboratory investigations.

The case manifested as the prominent progeroid disorders, multiple system (skin, skeleton, skeletal muscle, fat and nerve) degeneration and early–onset cystadenoma of the ovary. The case's presentation could be classified as a novel laminopathy which manifested as an overlapping phenotype among Charcot–Marie–Tooth disease, limb–girdle muscle dystrophy, Dunnigan–type familial partial lipodystrophy, mandibuloaral dysplasia, and atypical Werner syndrome.

Laminopathy is a rare disease which manifested as a wide clinical spectrum. Based on the clinical diagnosis, further study on candidate gene screening will help to elucidate the molecular mechanism.

To investigate the effect of rosiglitazone on the expression of fractalkine in renal cortex of type 2 diabetic rats.

Thirty Sprague–Dawley (SD)rats were randomly divided into normal control group (n=10) and type 2 diabetic model groups which were induced by intraperitoneal injection of low–dose streptozotocin combined with high fat diet. After diabetes established, diabetic rats were then randomized to receive rosiglitazone (n=10) or vehicle (n=10) treatment. Serum advanced glycosylation end products–peptide (AGE–P) was measured by using flow injection assay. The mRNA and protein expressions of fractalkine were detected by semi–quantitative reverse transcription polymerase chain reaction and immunohistochemical staining, respectively. One–way analysis of variances was used for data analysis.

The serum AGE–P[(2.87±0.21)U/ml], and the expression of fractalkine mRNA(1.41±0.03)and protein (0.79±0.04)in the renal cortex were significantly higher in the diabetes group than the normal control group [(0.90±0.13) U/ml, 0.85±0.04, and 0.46±0.03; P<0.01]. However, the serum AGE–P [(1.45±0.15) U/ml], and the expression of fractalkine mRNA (1.00±0.05) and protein (0.67±0.03) in the rosiglitazone group were significantly lower compared to the diabetes group (P<0.01).

Rosiglitazone may have renoprotective effects via inhibiting fractalkine expression in the renal cortex.

To investigate P213S gene polymorphism of L–selectin in people of Han and Dongxiang nationalities in Gansu Province and its association with type 2 diabetes.

A total of 143 patients with type 2 diabetes and 152 healthy controls of Han nationality and 116 patients with type 2 diabetes and 126 healthy controls of Dongxiang nationality were enrolled in this study during 2006 and 2008. Genotype of P213S was determined by polymerase chain reaction–ligation diction reaction. Plasma glucose, insulin, and lipid levels were measured by biochemical technique. χ ² test was used for data analysis.

L–selectin genotype frequencies of PP, PS, and SS were 55.9%, 37.8%, and 6.3% in type 2 diabetic patients of Han nationality; 41.4%, 50.7%, and 7.9% in normal controls of Han nationality; 44.8%, 48.3%, and 6.9% in type 2 diabetic patients of Dongxiang nationality; 38.1%, 44.4%, and 17.5% in normal controls of Dongxiang nationality. Allele frequencies of P or S were 74.8% and 25.2% in type 2 diabetic patients of Han nationality, 66.8% and 33.2% in normal controls of Han nationality, 69.0% and 31.0% in type 2 diabetic patients of Dongxiang nationality, 60.3% and 39.7% in normal controls of Dongxiang nationality (all P<0.05). The risk of type 2 diabetes of P allele carriers was 1.479 or 1.462 times of S allele carriers in Han or Dongxiang nationality.

L–selectin P213S polymorphism might be associated with type 2 diabetes, and P allele seems to be a risk factor of the disease.

To investigate the recruitment of different methods of bone mesenchymal stem cell (MSC) transplantation on diabetes.

A total of 54 diabetic rats were divided randomly into three groups: control group (n=18), tail vein MSCs transplantation group (n=18), and heart MSCs transplantation group (n=18). MSCs were isolated from bone marrow by adhesive screening method in aseptic condition, cultured and marked with 5–bromo–2–deoxyuridine (BrdU) in vitro. The blood glucose and body weight were measured at 3, 7 or 14 days. The pancreas was collected for hematoxylin and eosin (HE) staining and immunohistochemistry. The area of pancreatic islets and the values of IOD of yellow positive insulin granules were analyzed, and the distribution of BrdU positive MSCs in the pancreas was observed.

There were no significant difference in blood glucose level between the three groups at any time point. The body weight of tail vein MSCs transplantation group and heart MSCs transplantation group increased after MSCs transplantation. At 7 and 14 days, the difference in body weight was statistically significant between the three groups (F=5.0 or 4.8, P<0.05). At 7 days, the pancreatic islet area in heart MSCs transplantation group was increased, in comparison with the control group (F=4.50, P<0.05). At 14 days, insulin expression in tail vein MSCs transplantation group and heart MSCs transplantation group was significantly increased than the control group (F=4.613, P<0.05). Some BrdU–positive cells were observed in the pancreas.

Heart MSCs transplantation could play an important role in effective treatment of diabetes mellitus.

To investigate the relationship between early–phase insulin secretion and blood glucose variability in subject with normal glucose regulation.

Three hundred and thirty–nine individuals with normal body weight and normal glucose regulation, including 169 males and 170 females ranging from 20 to 69 years, were recruited from 10 hospitals in China. The mean amplitude of glycemic excursions (MAGE) observed by continuous glucose monitoring system was used assessing blood glucose variability. ΔI ₃₀/ΔG₃₀ during oral glucose tolerance test was used to assess early–phase insulin secretion, whereas baseline insulin secretion by HOMA–β. Insulin sensitivity was evaluated by HOMA–IR and insulin sensitivity index (ISIc)resulting from Cederhom formula.

The mean of MAGE in 339 normal subjects was (1.92±0.89)mmol/L. According to quartiles of MAGE, the subjects were divided into 4 groups, namely the Group A (MAGE < 1.33 mmol/L), Group B (MAGE 1.33 ~ 1.72 mmol/L), Group C (MAGE 1.73 ~ 2.41 mmol/L), and Group D (MAGE >2.41 mmol/L). Adjustment for age, sex and HOMA–IR, the ΔI ₃₀/ΔG₃₀ levels of Group A and B were both higher than those of Group C and D (P<0.05). There were no difference in HOMA–β, HOMA–IR and ISIc levels among the four groups (P>0.05). Spearman correlation analysis showed that the MAGE level was positively correlated with age (r=0.157, P=0.004), and negatively correlated with ΔI ₃₀/ΔG₃₀ (r=–0.270, P<0.001). Multiple regression analysis indicated that the ΔI₃₀/ΔG₃₀ was the independent influential factor of MAGE (β=–0.246,P<0.001).

The blood glucose excursions in subject with normal glucose regulation may be closely related to the function of early–phase insulin secretion.

To investigate the effects of inhibition of excessive insulin secretion on lipid metabolism and beta–cell functions in high–fat feeding rats following diazoxide intervention.

During May 2007 and July 2008, 30 male SD rats (10–week old) were randomly divided into the normal control group (n=10; normal diet), high–fat diet group (n=10; high–fat diet), and diazoxide group (n=10; high–fat diet+ 30 mg·kg^–1·d^–1 diazoxide). At 8 weeks, intra–peritoneal glucose tolerance test was conducted, and serum levels of free fatty acid and triglyceride and triglyceride components in the liver or skeletal muscle were measured. Expression of ACC1 mRNA and L–CPT1 mRNA was investigated using real–time polymerase chain reaction. One–way analysis of variances and Student–Newman–Kewls test were used for data analysis.

In intra–peritoneal glucose tolerance test, the insulin area under the curve was decreased in the high–fat diet group compared with the normal control group, while diazoxide intervention attenuated the decline (F=15.73, P<0.01). The plasma triglyceride and free fatty acid and triglyceride component in the muscles or liver were increased in the high–fat diet group, although diazoxide reversed these changes. High–fat diet alone increased the expression of ACC1 mRNA in the liver, which could be prevented by diazoxide (F=3.71, P<0.05). The expression of CPT1 mRNA in the liver or muscles was induced by high–fat diet, and diazoxide enhanced this effect (F=3.61, P<0.05;F=4.93, P<0.05).

Diazoxide may inhibit excessive insulin secretion and preserve pancreatic beta–cell function. Moreover, diazoxide could improve fatty acid metabolism and reduce fat accumulation in the liver and muscles, so as to decrease plasma levels of triglyceride and free fatty acid.

To explore the relationship between fasting plasma glucose (FPG) and acute insulin secretion stimulated by arginine.

A total of 626 adults [normal glucose tolerance (n=114), impaired glucose tolerance (n=60), and newly diagnosed type 2 diabetes mellitus (n=452)] were enrolled in this study from 2004 to 2005. All the participants received oral glucose tolerance test and arginine stimulation test. FPG, proinsulin (PI), and true insulin (TI) were measured. Acute insulin release function (ΔTI) and HOMA–IR were assessed. Covariance analysis and non–parameter test were used for data analysis.

ΔTI increased from 34.13 to 41.50 mmol/L when FPG was 3.8 to 5.0 mmol/L and reached the peak of 41.50 mmol/L when FPG was 5.0 mmol/L, then decreased gradually with FPG increasing. When FPG was 6.1 to 10.0 mmol/L, ΔTI reached the platform and decreased by about 35% compared with the peak ΔTI. When FPG was >10.0 mmol/L, ΔTI descended abruptly. ΔTI declined by about 60% when FPG was >11.1 mmol/L. PI gradually increased from 0.01 to 6.96 pmol/L when FPG was 3.8 to 10.0 mmol/L. However, PI decreased when FPG was >10.0 mmol/L. Insulin resistance index (HOMA–IR) was elevated with the increase of FPG. When FPG was >7.8 mmol/L, HOMA–IR remained high (6.82) and reached the platform.

Acute insulin release stimulated by arginine was relatively stable when FPG was 6.1 to 10.0 mmol/L, suggesting detectable reserved β cell function. Both ΔTI and PI were significantly decreased in the arginine stimulation test when FPG was >10.0 mmol/L, indicating that the acute insulin release function might be severely damaged.

Type 1 diabetic patients account for 5% of the total number of diabetic patients in China, and most of them occur in children and adolescents. From 1997 to 2000, the average annual incidence rate of type 1 diabetes among children in Beijing was 1.014/100,000^[1]。 The incidence of ketoacidosis is 3% ~4% per year^[2]It has a huge impact on the growth, development and quality of life of patients, and increases the family and socio-economic burden. The advent of subcutaneous insulin continuous infusion device (CSII) provides an effective means of strict glycemic control for patients with type 1 diabetes. However, if this technique is not properly mastered, ketoacidosis will easily occur^[3]。 Early detection of ketosis can avoid the occurrence of severe ketoacidosis. Traditional urinary ketone measurement is acetoacetic acid, but β-hydroxybutyric acid (β-OHB), which is obviously elevated in the compensatory stage of ketoacidosis (ketosis stage), cannot be detected. However, rapid blood ketone measurement can conveniently measure peripheral blood β-OHB. We observed the onset time of ketosis in patients with type 1 diabetes who were short-term interrupted from CSII therapy, and evaluated the clinical practical value of rapid blood ketone measurement.

As we all know, obesity can lead to insulin resistance and type 2 diabetes, but insulin resistance, type 2 diabetes and metabolic syndrome can also occur in people with normal weight or even thin weight, which is often difficult to understand. In fact, adipose tissue can not only regulate the body's energy balance, but also an important endocrine and metabolic regulatory organization. Adipose tissue is involved in the regulation of reproductive, hematopoietic and immune system functions by secreting various hormones and adipocytokines (including leptin, resistin, tumor necrosis factor-alpha, adiponectin, angiotensinogen and plasma plasminogen activator inhibitor-1, etc.). Previous Studies^[1,2]It was found that compared with the increase of adipocyte volume, the relationship between the abnormal differentiation of adipocyte and insulin resistance is more closely, which is the main culprit of the disorder of sugar and lipid metabolism in the body.

In 1918, Watanabe CK, a scientist at Yale University in the United States, discovered that guanidines in plants can reduce urine sugar concentrations and target goat beans^[1]。 In 1957, metformin produced by Bristol-Myers Squibb Company in the United States was approved for clinical use as a hypoglycemic drug for the first time in France. Half a century has passed, and metformin is growing stronger. Compared with other "upstart" drugs (e.g. thiazolidinediones, α-glycosidase inhibitors), metformin, which is cheap and effective, still has a broad market. As a developing country with large population, low economic income and abundant plant resources, China should pay attention to discovering and extracting effective ingredients from botanical medicines (especially traditional Chinese medicine), and actively serve the majority of patients. This article will briefly describe the research progress of antidiabetic botanical monomers, in order to provide useful reference for the research and development of related Chinese herbal medicines.

Islet β cell dysfunction and insulin resistance are important pathophysiological mechanisms in the pathogenesis of type 2 diabetes. At different stages of the disease, the manifestations and effects of these two factors are slightly different, but the view that "any hyperglycemia is insulin deficiency" suggests that clinical hyperglycemia only occurs when beta cells have severe functional defects (quality and quantity) and cannot maintain glucose metabolic homeostasis. The study of β cell function has been paid more and more attention by scholars, and improving β cell function has attracted increasing attention in the field of diabetes treatment.

polycythemia vera is a myeloproliferative disease dominated by clonal polycythemia, and its etiology and pathogenesis are not yet clear. The use of interferon-α (IFN-α) alone or in combination with chemotherapy can significantly improve the clinical symptoms of patients, reduce the number of bleeding and the dose of chemotherapy drugs^[1]。 This article reports a rare case of type 1 diabetes mellitus (T1DM) induced during IFN-α treatment in a patient with polycythemia vera.

Life is the basic characteristic of living things. Information, energy and matter are the three essential elements of life activities. The reason why life can continue lies in the constant exchange of information, energy and matter between organisms and the environment, and the metabolism. The dynamics of biological evolution come from the interaction between organisms and the environment. Metabolism is the premise and guarantee of the emergence and evolution of living organisms, and it is the "housekeeping" function retained in the long-term evolution process of human beings.

The incidence of hyperglycemia was higher in emergency patients. Studies have shown that hyperglycemia, especially severe hyperglycemia, is associated with mortality in a variety of critically ill patients. Although several professional organizations recommend that critically ill patients should strictly control blood glucose, this is controversial in clinical trials, systematic reviews, and meta-analyses. To this end, a parallel-group randomized controlled trial was conducted in 42 hospitals in Australia, New Zealand and Canada. The researchers randomly divided adult patients who received continuous treatment in the medical and surgical intensive care unit (ICU) for ≥3 days into two groups. One group underwent intensive blood glucose control with a target blood glucose range of 4.5~6.0 mmol/L, and the other group underwent traditional blood glucose control with a target blood glucose range of ≤10.0 mmol/L. The primary study endpoint was all-cause death within 90 days of randomization. A total of 6104 patients were randomized, of which 3054 received intensive glycemic control and 3050 received traditional glycemic control. At day 90, primary study data were obtained for 3010 and 3012 patients in both groups, respectively. The results showed that the baseline characteristics of patients in the two groups were similar, with 829 patients (27.5%) died in the intensive glycemic control group and 751 patients (24.9%) died in the traditional glycemic control group (the hazard ratio of intensive glycemic control was 1.14, the 95% confidence interval was 1.02-1.28,P＝0.02)。 There was no statistically significant difference in efficacy between surgical patients (surgery) and non-surgical patients (medication) (risk ratio of death in the intensive glycemic control group was 1.31 and 1.07, respectively,P＝0.10)。 Of the 3016 patients in the intensive treatment group, severe hypoglycemia (blood glucose level ≤2.2 mmoL/L) occurred in 206 patients (6.8%); Of the 3014 patients in the traditional glycemic control group, only 15 patients (0.5%) developed severe hypoglycemia (P<0.001)。 Patients in both groups were admitted to ICU (P=0.84) or days of hospital stay (P=0.86), performing dialysis (P=0.56) or days of renal replacement therapy (P=0.36) were not statistically significant. This international large-scale randomized clinical trial shows that intensive glycemic control can increase the mortality of adult patients in ICU, and glycemic control at ≤10.0 mmol/L can reduce the mortality of critically ill patients. – – Translated from Intensive versus conventional glucose control in critically ill patients. N Engl J Med, 2009, 360:1283 – 1297.

Both a low-fat vegetarian diet and an absolute vegetarian diet were associated with decreased body mass, improved insulin sensitivity, and reduced cardiovascular risk factors. Because cardiovascular disease is one of the early causes of death in diabetic patients, the potential cardiovascular benefits of vegetarian and absolutely vegetarian diets are particularly important, while their cardiovascular protective effects are similar in diabetic and non-diabetic individuals.

The UKPDS study showed that metformin hydrochloride has cardiovascular protective effects. However, its research design and analysis of results are still controversial, and its protection mechanism is still unclear. Studies have shown that it may be related to reducing body mass, reducing hyperinsulinemia, improving endothelial function and fibrinolytic state, reducing inflammatory response, reducing oxidative stress and glycation products, etc. However, this conclusion needs to be confirmed by clinical randomized studies. At present, several short-term studies of metformin combined with insulin in the treatment of patients with type 2 diabetes have shown that metformin can improve blood sugar control, reduce insulin requirements, and reduce the side effect of weight gain. However, the long-term effects of metformin treatment in patients with type 2 diabetes have not been reported.

Although insulin analogs have been widely used in the treatment of diabetic patients, it is inconclusive whether they are the best choice. To this end, the researchers conducted a meta-analysis on the efficacy and safety of insulin analogs and traditional human insulin in the treatment of type 1 diabetes, type 2 diabetes and gestational diabetes.

Studies have confirmed that the increase of urinary albumin excretion rate is closely related to the occurrence and development of diabetic nephropathy and macrovascular disease in patients with type 1 and type 2 diabetes, while the increase of urinary albumin excretion rate is related to hyperglycemia and hypertension. The Diabetes Prevention Program (DPP) is a prospective randomized clinical trial whose objective is to verify which treatment strategies can prevent or slow the transition to type 2 diabetes in people with impaired glucose tolerance who are older than 25 years of age, overweight or obese. The results of previous DPP studies showed that lifestyle intervention and metformin drug treatment can significantly delay the occurrence of type 2 diabetes. In this study, the changes in urinary albumin excretion rate of participants before and after the DPP study were observed.

In 1976, the famous human geneticist James Neel named a chapter in his book "Diabetes: A Genetic's Nightmare". Indeed, in the past 30 years, scholars have found that the phenotype and genotype of diabetes are highly heterogeneous when revealing various typical symptoms after impaired glucose homeostasis due to different causes. In recent years, with the acquisition of specific information such as human genome structure and variation, and the advent of high-throughput reading information technology, it is possible for geneticists to reveal the implicit genetic background underlying these symptoms. In this study, the researchers summarized and updated the latest advances in the genetics of type 1 diabetes onset and its application prospects in predictive and interventional treatments.

At present, the mechanism of physiological reverse regulatory response after hypoglycemia in type 2 diabetic patients receiving intensive therapy is still unclear. Stephen et al. from Tennessee, USA, tested the following two hypotheses through a 6-month intensive treatment with oral hypoglycemic drugs and a hypoglycemia clamp trial: (1) After 6 months of intensive treatment, patients whose glycosylated hemoglobin (HbA1c) dropped below 7.0% will blunt their autonomic response to hypoglycemia; (2) Previous hypoglycemia in patients with poor or good blood sugar control will cause the body to fail to reverse regulate subsequent hypoglycemia. Fifteen type 2 diabetic patients (8 males and 7 females) whose HbA1c was reduced to 6.7% after 6 months of combined therapy with metformin, glipizide controlled-release tablets and acarbose were enrolled in the study. These patients underwent a 2-day repeated hypoglycemic clamp test before and after hypoglycemic therapy. Eight non-diabetic controls received only one 2-day repeated hypoglycemic clamp test.

The seventh meeting of the China Group on Insulin Secretion (CGIS) was successfully held in Kunming on April 11, 2009, with the theme of "Revisiting the Function of Pancreatic Islet β Cells and Examining Blood Glucose Control and Vascular Complications". CGIS consultants, group leaders and deputy group leaders (professors Li Guangwei, Zhou Zhiguang, Ning Guang and Jia Weiping) and more than 60 insulin secretion research experts were invited to attend the meeting, of which eight experts gave special presentations, which are briefly introduced.

Diabetes mellitus is a clinical syndrome characterized by elevated blood glucose, and its etiology is diverse and complex. In order to provide family specimens and data that meet the requirements of molecular etiology, pathophysiology and clinical research of diabetes mellitus, the collection of diabetic families has been carried out at home and abroad since the 1980s. The extensive collection of diabetic families not only provides a guarantee for studying the relationship between genetic variation and clinical phenotype of single gene mutation diabetes, molecular etiology and pathogenesis of polygenic diabetes (common type 2 diabetes), but also provides the possibility for further research on rare and rare genetic diabetes.

The hospital where I trained as a resident established the Diabetes Metabolism Center early on. I can't remember how many lives we saved there in a row, but I am convinced that at the time, that number must have been close to the world record. At least, that's how it should have been until I transferred into the Army Medical Corps and met Amy.

The function of pancreatic islet β cells plays an important role in the progression of diabetes, and the dynamic changes of its "quality" and "quantity" have a decisive influence on the regulation of blood sugar and the occurrence of chronic complications. At present, in the treatment strategy of diabetes, it not only emphasizes the control of blood sugar to the standard to reduce the risk of microvascular and macrovascular complications such as eyes, kidneys and nerves, but also pays attention to the protection of pancreatic islet β cell function to achieve lasting and stable control of blood sugar. Therefore, understanding the biological characteristics of insulin synthesis and secretion by islet β cells, exploring the causes and mechanisms of islet β cell dysfunction, and mastering the detection methods of islet β cell function in clinical and research work will undoubtedly help to improve the diagnosis and treatment level of diabetes. "If a worker wants to do his job well, he must first sharpen his tool." Studying the function of pancreatic islet β cells is the "sharp tool" to achieve the goal of high-efficiency prevention and treatment of diabetes.

Type 2 diabetes is a chronic metabolic disease involved in multiple genes and environmental factors. Peripheral insulin resistance, functional decline of islet β cells and apoptosis are the pathophysiological basis of type 2 diabetes. It is generally believed that insulin resistance is the initiating factor of type 2 diabetes, and the functional decline and apoptosis of islet β cells are the determinants of type 2 diabetes.

Impaired islet beta cell function and insulin resistance are two key factors in the pathogenesis of type 2 diabetes. But which factor is more important is debatable.