Volume 04 · Issue 06 · 2012

With the rapid development of economy, the human lifestyle has undergone great changes, and the human disease spectrum has also undergone great changes. The incidence of complex diseases and chronic diseases (including cardiovascular diseases, diabetes, etc.) has increased significantly. The change of disease spectrum puts higher requirements on medical research. Traditional medical research is mainly based on single-factor research. At the same time, basic research and clinical research are seriously disconnected-on the one hand, a large number of basic research results cannot be effectively applied to clinical practice; On the other hand, the problems arising from clinical research cannot be fed back and solved in time, and there is a huge contrast between a large number of basic scientific research results and limited clinical benefits. In recent years, with the increasing maturity of multidisciplinary intersection, integration and collaboration, translational medicine has begun to attract the common attention of basic scientific researchers and clinicians. It is hoped that translational medicine can serve as a bridge between basic research and clinical applications, making the two-way transformation of experimental bench-clinical possible.

Translational medicine is considered to be a bridge between basic and clinical disciplines, requiring both bench-to-bedside^[1]And requires bedside to bench^[2], is a two-way process from basic discipline to clinical application, connecting basic and clinical^[3,4]It is a circular research system^[2]。 The reason why translational medicine has received great attention in recent years is that the process of transforming basic research results into clinical applications is too arduous and long. By conducting translational medicine research, adopting a systematic approach to translational medicine, integrating multi-disciplinary talents and resources, and breaking the artificial barrier between basic medicine and clinical medicine, preventive medicine, drug research and development, and health promotion, the translational process will be greatly accelerated.

To assess the positive rate and characteristics of cardiovascular autonomic neuropathy (CAN) in patients with newly diagnosed type 2 diabetes and to compare Ewing test with heart rate variability (HRV) for identifying CAN.

Ninety newly diagnosed type 2 diabetic patients (diabetic group) and 40 healthy subjects (control group) were enrolled from Department of Endocrinology and Metabolism of 4 hospitals in Guangdong Province(the Third Affiliated Hospital of Sun Yat-sen University, the First Affiliated Hospital of Shantou University Medical College, Guangdong General Hospital, Zhujiang Hospital of Southern Medical University). The diabetic group included 58 males and 32 females, with an average age (47±1) years. The control group included 21 males and 19 females, with an average age (45±2) years. Standard Ewing test and Holter (HRV analysis) were used to evaluate CAN, and comparison of these two diagnostic methods was committed. Difference of measurement data was compared with t test or one-way ANOVA and rank sum test was used for ranked data.

(1) The results of Ewing test showed that the positive rate of CAN in newly diagnosed type 2 diabetic patients (22.2% (20/90)) was higher than that in the controls (7.5% (3/40), χ ²=4.12, P<0.05). The Ewing scores in the diabetic patients (92.5) were significantly higher than those in the controls (7.0,Z=-3.72, P<0.01). The indexes of Ewing test (including valsalva ratio, heart-rate variation during deep breathing, heart rate and blood pressure response on standing) in the diabetic patients(92.5) were higher than those in the controls (Z value was -2.99, -2.23, -1.99 and -2.36, respectively, all P<0.05). (2) HRV analysis showed that the positive rate of CAN in newly diagnosed type 2 diabetic patients (34.4%(31/90)), was higher than that in the controls (12.5%(5/40), χ²=6.66, P<0.05). HRV indices related to parasympathetic function(including standard deviation of all normal-to-normal (N-N) intervals (SDNN), standard deviation of the averages of N-N intervals in all 5 min segments (SDANN) and power in the low frequency range (LF) in the diabetic patients significantly decreased compared with those in the controls (t value was 2.06, 2.24 and 6.48, respectively, all P<0.05), but there was no significant difference in those related to the sympathetic function such as root mean square of successive differences in R-R interval(RMSSD), percentage of R-R intervals differing more than 50 ms from the preceding one(PNN50) and power in the high frequency range(HF) (t value was 0.27, 0.15 and 1.40, respectively, all P>0.05).

Both Ewing tests and HRV showed a higher positive rate of CAN in the newly diagnosed type 2 diabetic patients than that in the control group, and parasympathetic function was mainly damaged. More CAN patients were detected by HRV than by Ewing test.

To evaluate the effectiveness of estimated glomerular filtration rate (eGFR) equations in patients with type 2 diabetic kidney disease.

A total of 224 patients with type 2 diabetes mellitus (male 133, female 91, average age (60±13) y) who were treated during October 2007 and December 2010 in the Third Affiliated Hospital of SUN Yat-sen University were enrolled in this study. Serum creatinine (Scr) and cystadin-C (cysC) were tested. eGFR was calculated with abbreviated Modification of Diet in Renal Disease (MDRD) equation, Chinese equation, Cockcroft-Gault equation, Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, Ruijin equation, EPI-Cys1 equation, EPI-Cys2 equation and MacIsaac equation, respectively, and compared with ^99mTc-DTPA-GFR (sGFR) by Bland-Altman analysis, Pearson correlation and receiver operator characteristic (ROC) curve.

(1) In Bland-Altman analysis, consistency of EPI-Cys1, EPI-Cys2 and MacIsaac equations with sGFR was better than other equations, and all eGFRs were above the limit point. The slopes of EPI-Cys1, EPI-Cys2 and MacIsaac equations were 0.168, 0.183, and 0.186, respectively. The intercept of MacIsaac equation was smaller. (2) Bias of EPI-Cys1, EPI-Cys2 and MacIsaac equations were smaller than others. 30% or 50% accuracy rate of these three equations was above 60% and 85%. EPI-Cys1 and EPI-Cys2 equations underestimated actual GFR and other Scr-based equations overestimated GFR. (3) As to diagnosis of diabetic kidney disease, EPI-Cys1 and EPI-Cys2 equations were more sensitive (94%) and accurate (>88%). The cut-point of MacIsaac and Ruijin equations were 62.4 and 64.9 ml·min^-1·1.73 m^-2, closer to 60 ml·min^-1·1.73 m^-2.

All the equations shows bias in estimating actual GFR. Compared with the equations induced by Scr, CysC-based equations may be more accurate and efficient. All the equations should be amended when applying to patients with type 2 diabetes mellitus.

To study the serum adiponectin level in diabetic foot patients and to analysis its biological mechanisms.

From January 2008 to December 2010, 85 patients with diabetes mellitus (DM) were enrolled, including 55 patients with diabetic foot (DF)(30 non-gangrenous cases and 25 gangrenous cases) and 30 without diabetic foot. Thirty age- and gender-matched healthy volunteers were served as controls. Clinical characteristics such as body mass index(BMI), fasting plasma glucose(FPG), glycosylated hemoglobin A1c(HbA1c), high-density lipoprotein cholesterol(HDL-C), high sensitive C-creactive protein(hsCRP), urinary albumin excretion rate (UAER), ankle-brachial index(ABI), and intima-media thickness (IMT)were recorded. Serum level of adiponectin was measured by ELISA. Influences of statins treatment on serum level of adiponectin were compared between DM and DF groups. Differences of means between groups were compared by One-way ANOVA. Correlations between serum adiponectin and other parameters were analyzed by Pearson's correlation and multivariate stepwise regression.

Serum adiponectin levels were higher in DF patients than DM patients and controls ((9.7±5.3)vs(5.4±2.8) and (8.3±3.4)mg/L, F=8.65, P<0.01). In DF group, serum adiponectin levels were increased in agreement with the exacerbation of albuminuria((6.0±1.7)vs(9.0±3.4)and (11.7±4.4)mg/L,F=10.22, P<0.01). Serum adiponectin levels showed an increasing tendency by statins in DF group((10±6) vs(8±3)mg/L,t=-1.27, P>0.05). In DF group, the correlation analysis indicated that adiponectin level was negatively correlated with BMI (r=-0.314)and HbA1c(r=-0.329), while positively correlative with UAER (r=0.401), IMT(r=0.360) and HDL-C(r=0.441)(all P<0.05). In multivariate stepwise regression analysis, HDL-C and UAER were independent factors of serum adiponectin.

Serum adiponectin level was significantly increased in DF patients. HDL-C and UAER may be independent factors of serum adiponectin.

To evaluate whether fasting blood glucose(FBG) and lipids in the first trimester of pregnancy effect the onset and the delivery outcomes of gestational diabetes mellitus(GDM).

A total of 3923 pregnant women who underwent FBG, triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), uric acid(UA) and sensitive C reactive peptide (sCRP) tests at first trimester and a standard 75 g oral glucose tolerance test (OGTT) between 24 and 32 weeks of gestation during 2000 and 2009 in Beijing 306th PLA Hospital were measured in this retrospective analysis. The association of first trimester FBG, lipids, sCRP and UA with GDM and the delivery outcomes were analysed.

First trimester FBG ((4.4±0.6) vs(4.2±0.4) mmol/L, t=-6.91, P<0.05), TG((1.9±0.7)vs(1.7±0.8)mmol/L,t=-3.30, P<0.05) and sCRP((2.4±1.6) vs(2.1±1.7) mg/L,t=-2.65, P<0.05) were higher in GDM than those in non-GDM. First trimester FBG, TG and sCRP were positively correlated with glucose levels during OGTT. First trimester FBG was negatively correlated with the neonatal Virgiria Apgar score. With the rise in FBG, TG and sCRP of pregnancies in the first trimester and cesarean section rate were increased. For data of the 3923 pregnancies, GDM and the adverse delivery outcomes were associated with first trimester FG, TG and sCRP. For GDM, the odds ratios and 95% confidence interval (CI) were 2.07(1.59 to 2.69, P<0.05), 1.25 (1.07 to 1.46,P<0.05) and 1.09 (1.02 to 1.16,P<0.05); for neonatal respiratory distress, 2.13(1.43 to 3.16,P<0.05), 0.73(0.45 to 1.18,P>0.05) and 1.01 (0.87 to 1.19,P>0.05); for macrosomia (≥4000 g), 1.45(1.09 to 1.92,P<0.05), 1.18(0.97 to 1.44,P>0.05) and 1.06(0.98 to 1.14,P>0.05); for low birth weight baby (≤2500 g), 0.97(95%CI, 0.62 to 1.52, P>0.05), 1.35(1.06 to 1.70,P<0.05) and 0.97(0.83 to 1.13,P>0.05).

First trimester FBG, TG and sCRP were increased in GDM.Even in the normal range, the higher level of these indexes are the risk factors for GDM, and may affect the outcomes of delivery.

To investigate the effect of osteocalcin on function of β-cell in type 2 diabetic rats, and to analyze the relationship of metformin with osteocalcin, glucose, lipid and insulin metabolism.

Thirty-six healthy Sprague-Dawlay (SD) rats aged 8 weeks were randomly assigned to group A (n=12), B (n=12), and C (n=12). Those of group A were fed normally, while those of group B and C were fed with high-fat diet. At 8 weeks, 25 μg/g streptozotocin (STZ) was injected into abdominal cavity of rats in group B and C, and 25 μg/g sodium citrate solution was injected into rats in group A. At 10 weeks, oral glucose tolerance test (OGTT) was conducted, and the rats of group C were treated with 25 mg·kg ^-1·d^-1 metformin for 4 weeks. At 4, 8, 10 and 14 weeks, serum levels of osteocalcin, fasting plasma glucose (FPG), fasting insulin (FINS), insulin sensitivity index (ISI), triglyceride (TG), total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were tested. At 14 week, all the rats were killed, and the pancreatic tissue was observed under microscope. The expression of osteocalcin was detected by immunohistochemical method. One-way of variance, LSD t test and Pearson linear correlation were used for data analysis.

At 10 weeks, 19 diabetic rats were successfully established in group B and C. At 8 weeks, body weight, TG, TC, and FINS in group B and C were significantly higher than those in group A (F values were 86.04, 74.25, 13.12 and 157.65, respectively; all P<0.01), while HDL-C and ISI were lower (F values were 12.13 and 24.01, respectively; all P<0.01). At 14 weeks, in group B and C, osteocalcin in pancreas were significantly decreased (0.84±0.09, 2.55±0.24 and 3.17±0.08, respectively;F value was 12.14, P<0.05). Pearson linear correlation analysis showed that pancreas osteocalcin was negatively correlated with FPG, TG and TC (r values were -0.811, -0.699 and -0.733, respectively; all P<0.05), and positively correlated with serum FINS, ISI, and HDL-C (r values were 0.826, 0.414 and 0.706, respectively; all P<0.05).

Osteocalcin could promote islet β-cells insulin secretion in type 2 diabetes rats. Serum and pancreas osteocalcin in group C was higher than that in group B after intervention with metformin, which suggests that metformin may promote the secretion of osteocalcin.

To investigate the effect of glucagon-like peptide 1 analogue liraglutide on microRNA expression of db/db mice and rat insulinoma cell line(INS-1).

Twenty 4-week old male db/db mice were randomly assigned to receive a subcutaneous injection of liraglutide(300 ng/g bid)or normal saline (0.1 ml bid)(control group) according to random numbers table. Glycated hemoglobin (HbA1c) was determined before and after 8 weeks of intervention. At the end of the intervention, intraperitoneal glucose tolerance test (IPGTT) was performed. Beta cells proliferation rate was determined by using immunohistochemistry methods. INS-1 cells were cultured with 0.5 mmol/L palmitic acid for 0, 48, 72 h or treated by 100 nmol/L liraglutide for 12 h before 72 h of palmitic acid(0.5 mmol/L) culture. microRNA miR-375 and miR-34a expression were examined by real-time polymerase chain reaction(RT-PCR). The t test or ANOVA analysis was used for data analysis.

Compared with the control group, HbA1c in the liraglutide group was significantly lower (7.3%±0.3% vs 4.7%±0.6%, t=16.47, P<0.01); the glucose aera under curve in the liraglutide group was decreased significantly((4568±197) vs (1927±127) mmol·L^-1·min^-1,t=26.53, P<0.05), while insulin aera under curve was increased significantly ((1080±247) vs(2818±378)μg·L^-1·min^-1,t=7.73, P<0.05). Immunohistochemistry showed more insulin staining in single pancreas of db/db mice after liraglutide treatment than in the control group (1.40±0.30 vs 0.37±0.09,t=19.14, P<0.01). More Brdu-positive cells were observed in islets of liraglutide-treated mice than in control mice after intervention(2.40%±0.22% vs 0.73%±0.10%,t=4.97, P<0.01). Compared with control mice, the miR-375 expression of pancreas in liraglutide-treated db/db mice was reduced by 50%(1.1±0.3 vs 2.2±0.5,t=3.08, P<0.05) and miR-34a was reduced by 71%(1.1±0.3 vs 3.8±1.2,t=2.80, P<0.05). In addition, the miR-375 expression of INS-1 cells was up-regulated dose- and time-dependently in response to palmitic acid; and palmitic acid-induced miR-375 expression was suppressed by liraglutide in vitro(F=7.20, P<0.01).

Liraglutide may preserve beta-cell proliferation in response to lipotoxicity through a regulation of miRNA.

To investigate the effect of acute myocardial ischemia on myocardial angiogenesis in diabetic rats and its possible mechanisms.

A total of 52 clean male 8-week SD rats were enrolled in this study, twenty of the rats were fed with high lipid food stuff and intravenously injected with streptozotocin to establish type 2 diabetic model. The left anterior descending coronary artery in the successfully-established diabetes rats models and 16 healthy rats (as control group) were ligated to establish acute myocardial infarction model. And another 16 rats were given thoracotomy only(as sham group). As a result, 12 rats survived in the diabetic group, 13 in the control group, 14 in the sham group. Two weeks after artery ligation, the rats were sacrificed to harvest the cardiac muscle in the left ventricular infarct zone and adjacent regions. The immunohistochemistry was applied to detect microvascular density (MVD) around ischemic zones in the three groups. Western blotting was used to detect the expression of vascular endothelial growth factor (VEGF), VEGF signaling mediators (phosphorylated protein kinase B (p-Akt), endothelial nitric oxide synthase(eNOS), and phosphorylated eNOS(p-eNOS)) and endostatin. Statistical significance between groups was determined with one-way analysis of variance (ANOVA), SNK q test was performed to compare the means between either two test groups.

Compared with the control group, diabetic group had a significantly reduced MVD (19.7±3.8 vs 14.2±3.6, q=2.98, P<0.05) around the ischemic territory. The protein expression of VEGF in the control diabetic group were all significantly lower than that in the sham group(1.53±0.20, 0.89±0.12, and 0.65±0.23, respectively;F=6.52, P<0.01). Compared with those in the control group, the p-eNOS expression was down-regulated (0.49±0.09 vs 1.16±0.12,t=5.68, P<0.05) and the endostatin expression was up-regulated significantly (4.6±0.6 vs 2.3±0.4,t=8.63, P<0.05) in the diabetic group. There were similar protein expression of p-Akt and eNOS between the control and diabetic groups(t values were 3.02 and 2.78, respectively, both P>0.05).

Together with endostatin, VEGF signaling pathway may play an important role in reduced angiogenesis at multiple levels in diabetic myocardium.

To discuss the effects of endomorphins (EMs) on synthesis and secretion of vasoactive substances in human umbilical vein endothelial cells(HUVECs) under advanced glycation end products (AGEs) injury conditions.

HUVECs were stimulated with bovine serum albumin(BSA), AGEs-BSA, AGEs-BSA+ EMs (1×10^-5, 1×10^-6, 1×10^-7, and 1×10^-8 mol/L), AGEs-BSA+ EMs(1×10^-5 mol/L)+ naloxone, respectively. The HUVEC viability was measured by methylthiazolyte-trazolium (MTT) assay, contents of nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) were detected by colorimetric analysis, level of endothelin-1 (ET-1) was detected by enzyme linked immunoabsorbent assay (ELISA), expression of eNOS and ET-1 mRNA was measured by reverse transcription polymerase chain reaction (RT-PCR). Data were analyzed by one-way ANOVA and t test.

Compared with the cells incubated with AGEs-BSA, the cell viability was significantly enhanced in 1×10^-5 mol/L EM1 group (0.89±0.05 vs 0.67±0.02, t=9.86, P<0.05), while secretion of NO, secretion and mRNA expression of ET-1 was significantly decreased ((14.8±1.4) μmol/L, (0.85±0.01)μg/L, 10.6±0.7 vs (23.0±0.7) μmol/L, (0.99±0.01) μg/L, 25.6±1.6, respectively;t values were 13.18, 31.36, and 50.18, all P<0.05), mRNA expression and secretion of eNOS was significantly enhanced (0.35±0.00, (2.53±0.20) U/ml vs 0.05±0.00, (0.99±0.01) U/ml, respectively;t values were 16.80 and 21.50, both P<0.05). Similar results were found in other groups of EMs, and the differences were statically significant between the EMs and AGEs-BSA group (t=2.24 to 102.40, all P<0.05). There were no significant differences in above-mentioned indices between the AGEs-BSA+ EMs+ naloxone and AGEs-BSA group (t=0.56 to 2.05, all P>0.05), but significant differences were found between AGEs-BSA+ EMs+ naloxone and EMs groups(t=2.24 to 64.96, all P<0.05).

EMs has a certain protective effect on AGEs-BSA-induced injury in HUVEC, which can be blocked by naloxone.

Metabolic syndrome is a series of biochemical and clinical metabolic abnormalities mainly caused by insulin resistance. The main risk factors include obesity, diabetes or abnormal glucose tolerance, blood lipid metabolism disorder, hypertension and microalbuminuria, etc. Its essence is the aggregation of various metabolic risk factors of cardiovascular and cerebrovascular diseases in individuals^[1]。 With the increasing number of obese patients worldwide, the incidence of the above-mentioned diseases in a clustered state is increasing. chemerin is a recently discovered adipokine secreted by adipocytes that is highly expressed in adipose tissue. Recent studies have shown that abnormal endocrine function of adipose tissue is an important cause of insulin resistance, and chemerin, one of adipokines, has a certain relationship with obesity, insulin resistance and metabolic syndrome^[2,3]。 Domestic Guan Yaqun et al^[4]chemerin was found to be associated with several key indicators of metabolic syndrome (such as insulin resistance) in the Uygur population, but no similar situation has been reported in the Han population. In this study, we compared the changes of plasma chemerin levels between healthy Han people and people with metabolic syndrome, and explored the relationship between chemerin levels and various components of metabolic syndrome.

Osteocalcin is a specific marker to assess bone turnover rate and bone formation, and is involved in the regulation of energy metabolism and glucose and lipid metabolism. Glucose and lipid metabolism disorder is an important factor in the occurrence and development of atherosclerosis. Studying the relationship between osteocalcin and atherosclerosis is helpful to further study the mechanism of atherosclerosis, and provide new ideas for the prevention and treatment of cardiovascular diseases. This article will briefly describe the recent progress in the research of osteocalcin and the mechanism of atherosclerosis.

Adipose tissue is the body's energy storage organ. Recent studies have shown that adipocytes are important endocrine organs, which can secrete a series of cytokines and participate in the metabolism of substances and immune inflammation in the body. Complement C1q tumor necrosis factor-associated protein 1 (CTRP1) is a newly discovered adipocytokine associated with hypertension, glucose and lipid metabolism disorders and obesity. In this paper, the recent research status on the molecular biological characteristics of CTRP1 and its association with atherosclerosis risk factors is reviewed as follows.

common variable immunodeficiency (CVID) is a heterogeneous immunodeficiency syndrome with unknown etiology, characterized by varying degrees of hypoimmunoglobulinemia, repeated bacterial infections and various immunological abnormalities, which can involve the respiratory system, digestive system, blood system, etc., and is often accompanied by autoimmune diseases and malignant tumors. It is the second largest primary immunodeficiency disease after selective IgA deficiency^[1]。 Its etiology has not been fully understood, and the World Health Organization defines it as combined immunodeficiency disease. Patients often have a long course of disease, diverse clinical manifestations, and are prone to clinical misdiagnosis and misdiagnosis. According to foreign literature reports, individual CVID patients can be complicated with diabetes, but it is rarely reported in China. A case of CVID complicated with diabetes mellitus admitted to our hospital is reported, and relevant literature is reviewed, aiming at making clinicians know about this coexistence and avoiding misdiagnosis and misdiagnosis.

Obesity, insulin resistance, and islet beta cell failure are the main features of type 2 diabetes mellitus (T2DM). Alterations in cytokines can lead to obesity-induced insulin resistance. Understanding the relationship between adipokines and obesity and glycemic control is beneficial to improve the prognosis of T2DM. The purpose of this study was to observe the effects of obesity and glycemic control on serum levels of retinol-binding protein 4 (RBP-4), lipocalin 2 (LCN-2), insulin-like growth factor-1 (IGF-1), insulin-like growth factor-binding protein-3 (IGFBP-3) and their relationship with islet β cell function in patients with T2DM.

Gastric bypass (BGP) can lead to weight loss and remission of type 2 diabetes in patients, but the mechanism is not fully understood. Previous studies have shown that this phenomenon may be related to the decrease of ghrelin and the increase of postprandial glucagon-like peptide-1 (GLP-1) and YY peptide. Gastro-acidmodulin (OXM) is a dual stimulant of GLP-1 receptor and glucagon receptor, which can reduce food intake, reduce weight, and improve blood sugar homeostasis. This study aimed to clarify whether OXM plays a role in weight loss and improvement of glucose metabolism after gastric bypass surgery.

Dendritic cells (DCs) may be involved in the formation of atherosclerosis, but their role remains unclear. The aim of this experiment was to investigate the interaction of DCs and monocyte-derived dendritic cells (Mo-DCs) with coronary artery smooth muscle cells (CASMCs) in the blood circulation of obese patients with type 2 diabetes mellitus (T2DM).

Increased hormone and cytokine production and decreased insulin sensitivity in patients with abdominal obesity lead to endothelial dysfunction. Hyperinsulinemia is considered an independent risk factor for ischemic heart disease and endothelial dysfunction in healthy people. In this study, the homeostatic model insulin resistance index (HOMA-IR) was used to assess insulin sensitivity in patients without a history of cardiovascular disease, without other components of metabolic syndrome other than hyperinsulinemia, and non-diabetic obese patients, and further to understand its effect on endothelial function.

For patients with type 2 diabetes, lifestyle interventions can improve blood glucose and cardiovascular disease (CVD) risk factors in the short term, but long-term research data are lacking. This study aimed to investigate the effects of a 4-year lifestyle intervention on body weight, physical fitness, and CVD risk factors in patients with type 2 diabetes.

CYBAGene C242T polymorphism is associated with cardiovascular disease, but the available data are contradictory. A study conducted in a Brazilian population investigated the effect of this gene variant on metabolic factors of cardiovascular risk and hypertension.

Type 2 diabetes may be associated with an increased risk of developing multiple tumors and may lead to a decrease in patient survival. The purpose of this study was to confirm that the survival rate of patients with solid malignant tumors complicated with diabetes is reduced, and that metformin can affect the survival rate.

Type 2 diabetes is mainly characterized by insulin resistance and dysfunction of islet β cells, the latter manifested by defects in insulin signaling. We propose the hypothesis that the effect of insulin promoting sugar-stimulated insulin secretion (GSIS) is reduced in an insulin-resistant population.

Many factors can increase the risk of hepatocellular carcinoma (HCC). Recent studies have shown that type 2 diabetes can increase the risk of HCC, meaning that patients with type 2 diabetes can be used as a target population for cancer prevention. Metformin, as the first-line drug for type 2 diabetes, mainly acts in the liver. Several studies suggest that metformin and metformin can reduce the risk of HCC. Although many preclinical studies have shown that metformin can exert anti-cancer properties in many tissues, there is currently no study that directly confirms the role of metformin in preventing liver cancer.