Volume 01 · Issue 04 · 2009

About 100 years ago, in 1906, it was discovered that patients with liver cirrhosis could be associated with diabetes. In the first half of the 20th century, this concomitant condition has been referred to as hepatogenous diabetes. Subsequently, with the progress of liver disease research, a variety of clinical chronic liver diseases are often accompanied by diabetes or abnormal glucose tolerance. From time to time, scholars study the relationship between liver cirrhosis or various chronic liver diseases and diabetes with the topic of "hepatogenic diabetes". However, so far, in the clinical classification of diabetes published by most diabetes professional organizations in the world or proposed by scholars, although clinical diabetes such as endocrine diseases, autoimmune diseases and pancreatic (or exocrine pancreatic) diseases with diabetes have been recognized as a clinical type of diabetes, there is no consensus on whether liver disease with diabetes is regarded as a type. In the past ten years, the pathophysiology and pathology of various chronic liver diseases have been studied, and it has been clear that fatty liver, steatotic hepatitis, cirrhosis and hepatocellular carcinoma are an interrelated clinical development process, and the prevalence of diabetes at all stages of the process has increased and increased with the progress of the prevalence. The pathophysiological mechanism and clinical characteristics of diabetes associated with chronic liver disease were understood. And saw the complementary relationship between chronic liver disease and diabetes in the occurrence and development. These aspects are shown in this special issue. As far as diabetes is concerned, today it is necessary to sort out the existing understanding of the relationship between liver and glucose metabolism and chronic liver disease and diabetes, and then examine the exact significance of diabetes as a clinical entity associated with chronic liver disease.

The liver plays an important role in glucose metabolism and energy homeostasis because it is the main organ for the action and uptake and degradation of insulin. Physiologically, 30% to 60% of the glucose absorbed into the blood from the digestive tract is used in the liver to synthesize glycogen or convert into amino acids or fatty acids. Insulin promotes glycogen synthesis by hepatocytes and reduces gluconeogenesis, while increasing blood sugar uptake by skeletal muscle and reducing adipocyte breakdown. In the case of insulin resistance or insulin deficiency, the decomposition of adipose tissue increases, the free fatty acids entering the liver through the blood increase, and the release of hepatic gluconeogenesis into the blood increases accordingly, accompanied by the decrease of glycogen synthesis by the liver and blood glucose uptake by skeletal muscle. As a result, it can induce fat ectopia and cause blood glucose increase and diabetes. Although hepatogenous diabetes is not included in the existing 4 main types and 12 subcategories of diabetes, changes in liver glucose metabolism and insulin sensitivity in chronic liver disease are bound to lead to insulin resistance and hyperglycemia. On the other hand, diabetes and its underlying diseases can not only lead to non-alcoholic fatty liver disease (NAFLD), but also promote the process of liver fibrosis in other liver diseases, increase the incidence of liver cirrhosis and liver cancer^{[1,2,3,4,5,6]}It suggests that there may be a causal vicious circle between diabetes and liver disease. In view of the different clinical characteristics and outcomes of common diabetes mellitus and hepatic diabetes mellitus, it is of great significance to accurately classify and effectively prevent and treat liver disease combined with diabetes mellitus, both in terms of improving the prognosis of diabetes mellitus and liver disease. Therefore, it is urgent to strengthen the research on the heterogeneity of diabetes mellitus complicated with liver disease and its diagnosis and treatment.

Clinical research data and epidemiological investigations show that the prevalence of type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) has increased significantly in the past 10 years. NAFLD has become the most common liver disease, often coexisting with type 2 diabetes. As components of metabolic syndrome, compared with a single factor, the two can greatly increase the risk of cardiovascular disease, so they have received more and more attention^[1,2,3,4]。

nonalcoholic fatty liver disease (NAFLD) is a metabolic stress liver injury associated with insulin resistance and genetic susceptibility, which is a pathological manifestation of obesity and metabolic syndrome involving the liver. Obesity and metabolic syndrome can not only cause NAFLD, but also promote the progression of other liver diseases such as chronic viral hepatitis C (hepatitis C) and chronic viral hepatitis B (hepatitis B) and affect their efficacy. This article mainly reviews the relationship between metabolic syndrome, NAFLD and chronic hepatitis B and its mechanism.

hepatogenous diabetes is diabetes mellitus secondary to chronic liver disease^[1]。 Unlike type 1 diabetes mellitus, hepatic diabetes mellitus is characterized by significantly elevated blood insulin values after fasting and glucose loading, and low insulin sensitivity (insulin resistance). The pathogenesis may be that the liver glycogen synthesis capacity is reduced, the sugar supply is insufficient, at the same time, the pituitary growth hormone enhances the decomposition of fat, and the free fatty acid (FFA) is increased, both of which promote insulin resistance^[2]。 The pathogenesis and clinical characteristics are attributed to type 2 diabetes. About 50% to 80% of patients with chronic liver disease have impaired glucose tolerance, and 20% to 30% of them will eventually develop diabetes^[3]。

To investigate the influence of glucose metabolism disorders on complications of cirrhosis.

A total of 494 residence cirrhosis patients (293 males, 201 females, mean age 62±14 y) attending the Department of Gastroenterology of First People's Hospital from 1st January 2005 to 31th December 2007 was enrolled. The influence of glucose metabolism disorders on complications of cirrhosis was retrospectively analyzed. Quantitative data were ananylzed byt test. Categorical data were analyzed by χ ² test and OR were caculated. P vaule <0.05 was considered satistically significant.

In 494 cases of liver cirrhosis, 191 patients had glucose metabolism disorders while 303 patients were normal. In patients with glucose metabolism disorders, the rates of gastrointestinal hemorrhage and hypersplenism were 104/191 and 141/191 respectively, which were higher than those in the patients with normal glucose metabolism. The OR was 2.539 and 1.584 respectively (all P<0.05). After stratifying according to viral hepatitis and alcohol addiction, in patients who had glucose metabolism disorders without viral hepatitis and alcohol addiction, theOR of upper gastrointestinal hemorrhage and hypersplenism was 2.653 and 2.640 respectively (all P<0.05). In all of 3 different age groups (<50 y, 50 ~ 70 y, >70 y), glucose metabolism disorders could increase the risk of the upper gastrointestinal hemorrhage(theOR was 3.314, 2.233, 2.425, all P<0.01).

Glucose metabolism disorders is a risk factor of upper gastrointestinal hemorrhage and hypersplenism in cirrhosis patients, which is independent on viral hepatitis and alcohol addiction. After stratifying according to age, glucose metabolism disorders is still a risk factor of upper gastrointestinal hemorrhage.

To investigate the prevalence of metabolic syndrome (MS) in patients with chronic viral hepatitis B (HBV) infection or non–alcoholic fatty liver disease (NAFLD), and to determine the relationship between MS and the risk of fibrosis in those patients.

One hundred and thirty–six patients with chronic HBV infections and 110 NAFLD patients were retrospectively analyzed from January 2008 to June 2009 for the prevalence of MS. Histological and laboratory assessment was received. t or χ ² test was used for data analysis.

The prevalence of MS of the NAFLD group was significantly higher than that of the HBV infection group (49.1% and 11.8%, respectively; P<0.01). In the patients with chronic HBV infection, severity of fibrosis was associated with increasing body mass index (BMI), higher aspartate aminotransferase (AST), gamma–glutamyl–transpeptidase (GGT), severe necroinflammation, and MS. In NAFLD group, MS was more prevalent in patients with non–alcoholic steatohepatitis (NASH) than simple fatty liver (55.4% and 40.0%, respectively;P<0.01); severity of fibrosis was associated with MS, higher alanine transarninase (ALT), AST, GGT, and severe necroinflammation.

MS may be more prevalent in NAFLD patients, and might be associated with the severity of fibrosis in patients with chronic HBV infection or NAFLD.

To investigate the treatment effects of solo rosiglitazone and combining Vitamin C on non–alcoholic steatohepatisis in high–diet rats, and explore the possible mechanisms involved.

Normal male SD rats were randomly devided into 5 groups, normal control group(n=6), model group(n=6), rosiglitazone group (n=8), vitamin C group (n=8), and rosiglitazone combining vitamin C group (n=8). All rats were feded with high–fat diet. And all treatment groups were given rosiglitazone, vitamin C, rosiglitazone and vitamin C respectively at week 16. Triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), superoxide dismutase (SOD), malondialdehyde (MDA), and tumor necrosis factor (TNF–α) in serum were measured at week 24. Then all rats were sacrificed. Liver wet weight and viscera fat quality were measured. And observe the liver steatosis, inflammation and fibrosis by HE stain and Masson stain.

Compared with model group, TG in treatment groups were decreased significantly(TG in rosiglitazone group, vitamin C group and rosiglitazone combining vitamin C group were (0.49±0.27, 0.62±0.15, 0.45±0.23) mmol/L, TG in model group was (1.36±0.57)mmol/L, all P<0.01). The scores of liver inflammation in treatment groups were decreased significantly (the scores of liver inflammation in rosiglitazone group, vitamin C group and rosiglitazone combining vitamin C group were 3.00±0.60, 5.13±1.64, 3.00±1.23, model group's was 12.75±3.59, allP<0.01). And the scores of liver fibrosis in treatment groups were decreased significantly (the scores of liver fibrosis in rosiglitazone group, vitamin C group and rosiglitazone combining vitamin C group were 5.67±0.52, 5.75±1.39, 4.00±0.58, model group's was 11.80±1.10, allP<0.01). The scores of liver fibrosis in rosiglitazone combining vitamin C group were lower than other treatment groups (F=62.33, all P<0.01).

Rosiglitazone and combination therapy can improve nonalcoholic steatohepatitis in rats, and combination therapy had a better effect.

To assess efficacy and safety of glipizide/metformin hydrochloride combination tablets in patients with type 2 diabetes mellitus.

A multicenter, double–masked, parallel–group, double–mimic active–controlled study was peformed. 240 patients (43 new diagnoses, 197 oral mono–therapy)with lifestyle inventions and oral mono–therapy type 2 diabetes mellitus from 4 centers were enrolled in this study and blindly into the A group( n=120, glipizide combined with metformin hydrochloride) and the B group(n=120, glipizide/metformin hydrochloride combination tablets). The whole observation lasted for 12 weeks. The efficacy indicators measured include glycohemoglobin A1c (HbA1c), fasting plasma glucose and 2 hours postprandial plasma glucose and the safety parameters measure include renal and hepatic function, serum lipids, blood profiles, urea profiles and adverse events. The data of statistics were analyzed by non–inferiority evaluation.

After 12 weeks' treatment, the decreased values of HbA1c was 2.64%(A group) vs 2.68%(B group) in new diagnoses and 1.06%(A group) vs 1.26%(B group) in oral mono–therapy. Glipizide/metformin hybroch loride tablets also reduced fasting plasma glucose and 2 hours postprandial plasma glucose, Similar decrease in fasting plasma glucose, 2 hours postprandial plasma glucose and HbA1c were found in both A and B group without significant differences. No severe adverse events were noted. The hypoglycemia event reports were not significantly different between these two groups.

Glipizide/metformin hydrochloride tablets were similar efficacy and safety profiles with glipizide combined with metformin in patients with type 2 diabetes mellitus.

To compare the prevalence of metabolic syndrome in Heilongjiang adults under different definitions and find the appropriate diagnostic.

A cross–sectional study was conducted in Heilongjiang with a representative sample of 2875 Chinese adults from 20 to 74 years of age. The different prevalences under ATPIII, IDF and CDS definitions respectively were calculated and the results were compared by Kappa test.

The adjusted prevalences of metabolic syndrome under ATPIII, IDF, and CDS were 14.47%, 21.92% and 18.73%, respectively. The 87.58% concordance of metabolic syndrome cases was found between ATPIII and CDS, 84.97% between ATPIII and IDF, and 82.50% between CDS and IDF.

The prevalence of MS has been in a high level in the inhabitant in Helongjiang province between 20 and 74 years old. The agreement among three definitions is high.

To estimate the prevalence of glycometabolic abnormality among adults aged 40–79 years in Chengdu area in 2008.

A cross–sectional population survey for glycometabolic abnormality using randomly cluster– sampling was performed from April to November in 2008, questionaire and 75 gram oral glucose tolerance test (OGTT)were conducted in 5205 subjects.

Prevalence of diabetes mellitus, impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and impaired glucose regulation (IGR) were 18.0%, 2.5%, 20.1% and 22.6%, respectively. The prevalence of glycometabolic abnormality have no differences between sexes. The prevalence of diabetes and IGT increased with aging, but the prevalence of IFG have no obvious associated with age. Male, urban population, obesity, increase of diastolic blood pressure, TG and UA are risk factors for IGR. Increase of waist circumference, TG, TC, and decreasd of HDL–C are risk factors for diabetes in more than 40 year–old population of Chengdu area.

Our results showed that the glycometabolic abnormality are highly prevalent in Chengdu residents; over half of them are undiagnosed diabetes. The prevalence of diabetes increased with aging.

To assay serum retinol binding protein 4(RBP4) and advanced oxidation protein product(AOPP) levels in rats with diabetes and atherosclerosis, and to explore the correlation between RBP4 and Diabetic macroangiopathy.

45 healthy male Wistar rats in SPF level were randomly divided into 3 groups (n=15). Group A for the normal group, fed normal diet. Group B for diabetic atherosclerosis group. Group C for diabetes atherosclerosis intervention group plus telmisartan. Rats in group B and C were fed with high fat and high sugar diet, and to a one–time high–dose intraperitoneal injection of streptozotocin (STZ) and to vitamin D₃ orally, make the establishment of diabetic atherosclerosis model. Two mouths later, modeling success was confirmed, rats in group B were continued feeding high–fat and high–sugar diet, C group fed high–fat and high–sugar diet as well as simultaneously to telmisartan (5 mg·kg^–1·d^–1) gavage. Experiment lasted 16 weeks, all rats after fasting overnight, 10% chloral hydrate intraperitoneal anesthesia, centrifugal separation after the cardiac blood serum, automatic biochemical analyzer measured serum TC, TG, HDL–C, LDL–C. Enzyme–linked immunosorbent assay (ELISA) measured serum RBP4, UV spectrophotometer measured serum AOPP content. Execution of the rat abdominal aorta to do HE staining.

Surem TG, TC, LDL–C in group B increased than those in group A, and surem HDL–C reduced.But it is not obvious that surem TG, TC, LDL–C in group C increased and HDL–C were lower than group A. RBP4 and AOPP in group B were significantly higher, but group C significantly reduced after the intervention of telmisartan. RBP4 correlated with AOPP. Abdominal aortic HE staining showed in group B fibrous tissue of the artery intimal medial wall were hyperplasia, and some fibrosis and hyalinization, and calcification significantly. In group C artery intimal medial wall showed only slight fibrosis and hyalinization.

Based on the above results, we speculate that RBP4 may affect the blood lipid profile and intima enhanced oxidative stress involved in diabetic macroangiopathy of the occurrence and development.

To investigate the effects of spironolactone on podocytic adhesive capacity in type 1 diabetic rats.

Sixteen healthy male Wistar rats (180 to 220 g, 6 to 7 weeks old) were injected with STZ via a tail vein to induce type 1 diabetes, and 13 of them were randomly divided into the spironolactone treatment group (40 mg·kg^–1·d^–1 spironolactone gavage for 12 weeks, n=6) or the diabetic control group (distilled water alone, n=7). Another 6 body–weight–matched rats were served as the normal control group. On week 12, 24–hour urinary albumin, systolic blood pressure (SBP), and fasting blood glucose (FBG) were evaluated. Expression of integrin α3 was detected by immunohistochemistry and Western blot. One–way ANOVA with the Students–Newman–Keuls test as a post hoc test was used to evaluate significant differences between the groups.

Before the administration of spironolactone, FBG of the diabetic control group was significantly higher than that of the normal control group ((23.96±3.86) and (4.85±0.50) mmol/L, respectively; q=12.00, P<0.01); however, there was no significant difference between the diabetic group and the spironolactone treatment group ((23.96±3.86)and (22.76±3.85) mmol/L, respectively;q=0.95, P>0.05). SBP did not differ significantly between the three groups (F=0.51, P>0.05). At 12 weeks, rats received STZ alone revealed an increase in FBG ((28.54±2.24) and (5.20±0.19) mmol/L, respectively;q=54.39, P<0.01), which was not influenced by the treatment with spironolactone (q=2.73, P>0.05). SBP did not differ significantly between the three groups (F=0.18, P>0.05). Furthermore, 24–hour urinary albumin was significantly increased in the diabetic control group ((6.54±1.14) and (1.01±0.08) mg/d, respectively;q=19.50, P<0.01). In contrast, the spironolactone treatment group showed considerable improvement in urine albumin ((5.32±0.31) and (6.54±1.14) mg/d, respectively;q=4.30, P<0.05), as well as up–regulation of integrin α3 protein expression (0.48±0.62 and 0.28±0.62, respectively;q=8.11, P<0.01).

After the administration of spironolactone, the expression of integrin α3 was significantly increased in STZ–induced type 1 diabetic rats without affecting FBG and SBP, suggesting that beneficial effects of spironolactone on podocytic adhesion may be one of its protective mechanisms against diabetic nephropathy.

The liver, as the main target organ of insulin action, plays an important role in maintaining the production and output of endogenous glucose under fasting state and the absorption, utilization and storage of glucose after eating. Hepatic insulin resistance mainly refers to the decrease of the ability of insulin to inhibit liver glucose export, while cellular insulin resistance refers to the change of intracellular signal transduction after activation of intracellular insulin receptor^[1]It can be determined by measuring intermediate protein phosphorylation, alteration of intermediate kinase activity, and/or alteration in regulating target gene expression or target cell function upon insulin stimulation^[2]。

Pancreatic cancer is a malignant tumor of digestive system with hidden clinical symptoms, rapid development and poor prognosis. Due to the difficulty of early diagnosis, 80% ~90% of patients were in the middle and late stage at the time of consultation, and the surgical resection rate was only 15%^[1]。 It is very important to carry out early pancreatic cancer screening in high-risk groups to improve patient survival and prognosis. The latest data show that nearly 80% of pancreatic cancer patients develop hyperglycemia or diabetes in the early stage of tumor development, and most of them are new diabetes with a course of less than 2 years^[2]。 Therefore, the role of new-onset diabetes in the early diagnosis of pancreatic cancer has been paid more and more attention. This article will review the research progress in this field.

With the improvement of living standards and lifestyle changes, the incidence of diabetes in China is increasing year by year, and the number of diabetic patients is second only to India, ranking second in the world. Diabetes mellitus as a chronic metabolic disease can cause a variety of complications. In recent years, with the deepening of research, there is more and more evidence showing that there is a close relationship between diabetes and primary liver cancer.

congenital hyper-insulinism in infancy (CHI), also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or hyperinsulinism in infancy (HI), is a rare disease and the most common cause of persistent hypoglycemia in infants^[1]。 Its clinical features are persistent hyperinsulinemia with hypoketosomaemia, hypofatty acidemia, convulsions, convulsions, irreversible damage to the nervous system and even death. Infant congenital hyperinsulinism is a hereditary ion channel disease, and 8 genes (ABCC8, KCNJ11, HADH, GLUD1, GCK, HNF4A, SLC16A1, UCP2) have been identified to be related to its pathogenesis^[2]。 According to different genes involved, congenital hyperinsulinism in infants and young children can be divided into different subtypes, among which adenosine triphosphate (ATP) -sensitive potassium ion (K_ATP) channel involvement subtype (K_ATP-CHI) is most common, and the genes involved in this type include ABCC8, KCNJ11. This paper summarizes the research status of ABCC8 and KCNJ11 gene mutations.

The most basic feature of type 2 diabetes is chronic hyperglycemia, and the main pathophysiological basis is insulin resistance and/or islet beta cell dysfunction. Because diabetes does not necessarily occur in people with insulin resistance, the decrease of pancreatic islet β cell function is a prerequisite for the onset of diabetes. The decrease of the total amount of β cells is the pathological basis of the decrease of β cell function. The total amount of β cells in patients with type 2 diabetes mellitus is reduced by 50% at the time of diagnosis^[1]。 After a 1-year follow-up of healthy live pancreatic donors, it was found that half of the pancreas removed resulted in impaired glucose tolerance and insulin secretion^[2]This indicates that normal blood glucose levels can no longer be maintained when the total number of beta cells is reduced by half. Therefore, preventing or reversing the progressive decline in the total amount and function of beta cells can prevent the occurrence and progression of type 2 diabetes.

Diabetic neuropathy has a high prevalence, which can involve all parts of the human nervous system. It is the most important cause of non-traumatic distal limb amputation and the most important risk factor of diabetic foot ulcer. Every 30 seconds, one patient's lower limb is lost due to diabetes worldwide, and as many as 70% of patients with lower limb amputations are accompanied by diabetes. Diabetic foot is the most common cause of hospitalization for diabetic patients, costing approximately 40 percent of health expenses in developing countries, and the direct cost of amputation is estimated to be approximately $30,000 to $60,000.

In this study, intravascular ultrasound technique was used to compare the effects of three commonly used drug-eluting stent (DES) replantation strategies in the treatment of bare metal stent (BMS) -induced restenosis. The researchers used the following methods to reimplant 80 consecutive bare metal stent restenosis sites: the first type, direct implantation; The second type is implanted after low-pressure pre-expansion with a small balloon; The third is implanted using a semi-standard balloon with a diameter ≥ previous bare metal stent after high pressure pre-dilation. The second and third implantation modalities included more patients with diabetes mellitus. The stenosis site was relatively more proximal and more localized in those who received the first implant mode, while the stenosis was more severe in those who received the second and third implant modes. Drug-eluting stent size, parachute opening pressure, and postoperative angiographic results were similar in each group. The minimum area of stent area and the percentage of drug-eluting stent expansion were significantly greater in those who received the third implantation method than in those who received the first and second implantation methods ((6.4 ± 1.5), (5.6 ± 1.6), and (4.4 ± 1.4) mm, respectively²,P<0.001； (88±30) %, (74±14) % and (73±23) %, respectively,P＝0.021]。 Those receiving the third implantation method had only the smallest stent area after intervention for 3 lesions<5 mm²Whereas 14 received the first implant method and 11 received the second implant method (odds ratio 0.11, 95% confidence interval 0.03-0.38,P<0.001)。 In conclusion, the increase in lumen mainly depends on bare metal stent expansion, but the increase in bare metal stent lumen at the site of stenosis is most pronounced in those receiving the third implantation method. It can be seen that when drug-eluting stent implantation is used to treat vascular restenosis caused by bare metal stent, high pressure pre-dilation can improve the dilation effect of drug-eluting stent after interventional therapy independently of bare metal stent dilation. – – Translated from Impact of different re-stenting strategies on expansion of a drug-eluting stent implanted to treat bare-metal stent restenosis. Am J Cardiol, 2009, 104: 531 – 537.

In 2005, the heart failure guidelines developed by the American Heart Association/American College of Cardiology re-focused on high-risk patients and emphasized that heart failure is a progressive disease. By classifying patients according to different stages of heart failure and emphasizing individualized treatment, patients can be given the best evidence-based treatment in each stage of heart failure. Treatment targeting risk factors for left ventricular dysfunction or other symptoms can delay the progression of heart failure. Beta-blockers include a variety of drugs, and the selection of appropriate drugs is important for the treatment of all stages of heart failure. Beta-blockers are routinely used in patients with stage A heart failure complicated with hypertension. Recently, due to the metabolic side effects of certain beta-blockers, the use of any beta-blockers in diabetic patients has been unduly questioned. Beta-receptor blockade is the standard treatment in patients with stage B heart failure who have developed myocardial infarction, but little evidence has been reported for its use in patients with asymptomatic left ventricular dysfunction. In addition, beta blockers are one of the core treatment contents of patients with stage C heart failure and some patients with stage D heart failure. This review evaluates the use of beta blockers in various stages of heart failure through an evidence-based approach, thereby providing a better understanding of the use of beta blockers in patients with heart failure. – – Translated from Beta-blocker use for the stages of heart failure. Mayo Clin Proc, 2009, 84:718 – 729.

The recent cardiovascular endpoints of diabetic patients with acute ischemic chest pain are still inconsistent between experimental studies and clinical practice, while the long-term endpoints are lacking observational data. This cohort study was designed to identify near-and long-term cardiovascular endpoints in diabetic patients who develop acute ischemic chest pain. The researchers followed patients with acute ischemic chest pain who were registered for hospitalization in Olmestd Village, Minnesota, USA, between January 1, 1995, and December 31, 2002, for an average period of 16.6 years. The primary study endpoint was long-term all-cause mortality, and other study endpoints included death, myocardial infarction, stroke, revascularization (major malignant cardiovascular and cerebrovascular events), and heart failure at 30 days and 7.3 years. Of the 2271 eligible, 336 patients had diabetes mellitus. The results showed that the 30-day incidence of malignant cardiovascular and cerebrovascular events in diabetic patients and non-diabetic patients was 10.1% and 6.1%, respectively (P＝0.007)。 The incidence of heart failure at 30 d was higher in diabetic patients than in non-diabetic patients (9.8% and 3.1%,P<0.001)。 Diabetic patients were more likely to develop malignant cardiovascular and cerebrovascular events at 7.3 years than non-diabetic patients (71.2% and 45.1%, respectively, with an unadjusted hazard ratio of 2.15,P<0.001) and heart failure (45.1% and 18.2%, respectively, with 95% CI 1.87 to 2.48,P<0.001)。 During follow-up there were 272 deaths (81.9%) among diabetic patients and 936 deaths (49.2%) among non-diabetic patients (P<0.001)。 It can be seen that in patients with acute ischemic chest pain, diabetes is associated with an increased risk of recent malignant cardiovascular and cerebrovascular events and heart failure, and an increased risk of long-term death. Diabetes should be included as a high risk factor in the American guidelines for acute coronary syndromes. – – Translated from Usefulness of diabetes mellitus to predict long-term outcomes in patients with unstable angina pectoris. Am J Cardiol, 2009, 104: 492 – 497.

Data on the predictive value of blood glucose in admitted patients due to acute coronary (coronary) events are scarce. This study analyzed the fasting blood glucose levels of patients with acute coronary syndrome at admission provided by the Acute Coronary Syndrome Registry of the University of Michigan, USA, and divided their blood glucose levels into three layers: 0.7 to 1 g/L, 1 to 1.26 g/L,>1.26 g/L. Primary study endpoints included in-hospital and after 6 months mortality and composite endpoints (stroke, recurrent myocardial infarction, and death). The results showed that fasting blood glucose ≥1 g/L was associated with increased in-hospital mortality in 1525 patients with blood glucose records (29% of whom were diabetic). In patients without a history of diabetes, fasting blood glucose>1.26 g/L was associated with in-hospital adverse events (odds ratio, 3.37, 95% confidence interval, 1.51 to 5.71). Fasting blood glucose levels were associated with an increased risk of death after 6 months in non-diabetic patients (odds ratio 3.03, 95% CI 1.35-6.81 for fasting blood glucose 1-1.26 g/L; odds ratio 2.81, 95% CI 1.07-7.36 for fasting blood glucose>1.26 g/L), but fasting blood glucose levels in diabetic patients were not associated with an increased risk of death after 6 months. It can be seen that there is a strong correlation between admission fasting blood glucose and mortality in patients with acute coronary syndrome (especially in non-diabetic patients). – – Translated from Prognostic value of admission fasting glucose levels in patients with acute coronary syndrome. Am J Cardiol, 2009, 104: 470 – 474.

To clarify the individual differential factors affecting the antiplatelet effect of aspirin, the researchers determined the platelet response of aspirin in 745 healthy adults who took the drug for the first time. The study evaluated the body response to platelet arachidonic acid, ADP and collagen at baseline and after oral administration of 81 mg/d aspirin for 14 days by measuring whole blood agglutination. The boundaries of aspirin resistance cannot be determined due to wide individual variation in assay results. Individual differences in platelet response before and after aspirin administration are heritable. Women presented stronger ADP and collagen-stimulated platelet agglutination before and after aspirin administration, and aspirin had weaker inhibition of collagen-induced platelet agglutination (extent of inhibition of collagen-induced platelet agglutination: 49.9 ± 30.9 and 57.5 ± 42.5 for women and men, respectively,P＝0.005)。 If collagen-induced platelet agglutination capacity will be inhibited<70% as the cut-off point, then aspirin resistance would be 21% of the total population, with 30% of women and 16% of men. Aspirin-resistant people were older, had higher levels of total cholesterol and LDL cholesterol, lower hematocrit, and higher platelet counts than those who were relatively sensitive. In conclusion, this study shows that platelet function is heritable. The response of platelets to aspirin evaluated by whole blood platelet agglutination varied greatly among individuals, and aspirin resistance was more pronounced in women than in men. – – Translated from Aspirin resistance in healthy drug-naive men versus women (from the Heredity and Phenotype Intervention Heart Study). Am J Cardiol, 2009, 104: 606 – 612.

There is evidence that there is a link between taking antipsychotic drugs and new onset diabetes. However, the risk of taking antipsychotics in diabetics is unclear. In this study, a nested case-control design was used to select diabetic patients aged ≥66 years and who started taking antipsychotic drugs between April 1, 2002 and March 31, 2006, from the Ontario Population Health Database, Canada, with follow-up lasting from the start of medication until March 31, 2007. All subjects were divided into three groups: insulin-treated group, oral hypoglycemic drug-treated group and untreated group. The enrolled cases were patients admitted for hyperglycemia (including emergency admission and general admission), and the proportion of each case was ≤10 controls. To compare the risk of admission for hyperglycemia in patients currently taking classical or non-classical antipsychotics with those who had been off for more than 6 months. Results showed: Of the 13 817 patients included in the study, 1515 patients were admitted due to hyperglycemia. Patients currently taking antipsychotics had a higher risk of admission for hyperglycemia than those who had been withdrawn for some time (adjusted odds ratio 1.5%; 95% confidence interval 1.29 to 1.74). Patients taking antipsychotics have an increased risk of admission for hyperglycemia, especially in patients who have just started antipsychotic therapy. It can be seen that the beginning of antipsychotic treatment in elderly diabetic patients is associated with an increased risk of admission for hyperglycemia, and this risk increases more significantly in patients who have just started treatment; A variety of antipsychotic drugs can increase this risk. – – Translated from Antipsychotic drugs and hyperglycemia in older patients with diabetes. Arch Intern Med, 2009, 169: 1282 – 1289.

Patients with type 2 diabetes need more practical lifestyle interventions to help them increase physical activity and follow nutritional therapy guidelines. In this study, we compared the comprehensive guidance of physical exercise and low glycemic index food intake (first step first bite plan) with the simple increase of physical exercise (first step plan) to observe whether the former can more effectively improve the glycosylated hemoglobin level, various physical examination indexes and cardiovascular health endpoints in patients with type 2 diabetes. Study subjects were randomly assigned to the first step planning group (n=22) or the first step first mouth plan group (n=22), subjects were required to attend a weekly consultation for the first 4 weeks, followed by follow-up at weeks 5 to 16. During the study, the number of daily steps walked by all subjects was recorded, and the daily intake of low-glycemic-index foods was also recorded in the first step and first bite plan group. The results showed that at week 16 (each groupn=19), each patient in both groups walked approximately 3000 more steps per day compared to baseline (P<0.01)。 The waist circumference of the subjects in the first step plan group was reduced by (5.9 ± 0.9) cm, and the waist circumference of the subjects in the first step first mouth plan group was reduced by (3.7 ± 0.5) cm. The hip circumference of the two groups decreased (3.7 ± 0.6) cm and (2.2 ± 0.5) cm, respectively (bothP<0.01)。 There was no significant difference in physical examination and metabolic indexes (including glycosylated hemoglobin) between the two groups. The amount of physical exercise in both groups increased, and the daily intake of low-glycemic index foods in the first step and first bite group also increased. It can be seen that increasing the intake of low glycemic index things in patients with type 2 diabetes with good glycemic control on the basis of daily physical exercise did not improve their physical examination indexes and metabolic endpoints. To observe better clinical outcomes in the future, it is necessary to significantly increase the number of cases and extend the observation time limit for low-glycemic index food intake. – – Translated from The First Step First Bite Program: guidance to increase physical activity and daily intake of low-glycemic index foods. J Am Diet Assoc, 2009, 109: 1411 – 1416.

High cholesterol diets are associated with an increased risk of coronary atherosclerotic heart disease. However, it remains unclear whether all high-cholesterol foods increase the risk of heart disease. This study aimed to determine whether the consumption of shellfish food is associated with an increased risk of coronary atherosclerotic heart disease. The data were obtained from an atherosclerosis community study of middle-aged and elderly Americans. The study analyzed the association between the consumption of shellfish food and the development of coronary atherosclerotic heart disease. All subjects were divided into a group that consumed small amounts of shellfish food, a group that consumed moderate amounts of shellfish food, and a group that consumed large amounts of shellfish food. A total of 13 355 people met the inclusion criteria, of which 1382 had coronary atherosclerotic heart disease. The risk ratio of coronary atherosclerotic heart disease was 0.89 (95% confidence interval, 0.79-1.00) in the group eating medium shellfish food and 0.91 (95% confidence interval, 0.80-1.03) in the group eating large shellfish food compared to the group eating small shellfish food. After adjusting for age, sex, race, smoking status, body mass index, diabetes, hypertension, low-density lipoprotein cholesterol level, high-density lipoprotein cholesterol level, family history of early onset heart disease, and exercise status, the risk ratio of coronary atherosclerotic heart disease was 0.96 (95% confidence interval, 0.80-1.16) in the group eating moderate shellfish food and 0.98 (95% confidence interval, 0.82-1.18) in the group eating large shellfish food. – – Translated from Shellfish consumption and risk of coronary heart disease. J Am Diet Assoc, 2009, 109: 1422 – 1426.

Women with type 1 or type 2 diabetes have higher rates of infant perinatal mortality. Although high blood glucose levels may be related to this, the specific mechanism remains unclear. In order to clarify the causes of fetal or neonatal death in women with type 1 or type 2 diabetes, to know whether the causes of perinatal death of infants and young children are the same in women with type 1 diabetes and women with type 2 diabetes, and to determine the relationship between perinatal infant mortality and maternal glycemic control, the researchers retrospectively analyzed the medical records of women with type 1 diabetes and type 2 diabetes who had fetal death or neonatal death, respectively. The results showed that of the 93 perinatal deaths (59 type 1 diabetes, 34 type 2 diabetes), 73 were fetal, 12 early neonatal and 8 late neonatal deaths. Eighteen died of congenital anomalies, 64 died of asphyxia before delivery, four died of asphyxia during delivery, one died of unknown cause and one lacked detailed records. The mean gestational age was 34 weeks. The incidence of infant congenital abnormalities in mothers with type 1 diabetes was lower than that in mothers with type 2 diabetes (relative risk 0.37, 95% confidence interval 0.15-0.95). The highest value of glycated hemoglobin in mothers before and during pregnancy showed a curved relationship with birth weight: when the level of glycated hemoglobin was low, birth weight was normal; Birth weight exceeds normal when glycated hemoglobin levels are moderately elevated; Extremely elevated levels of glycated hemoglobin are associated with severe intrauterine growth retardation. It can be seen that hyperglycemia can not only induce fetal macrosomia, but also lead to vascular abnormalities, thus affecting the blood supply to the uterus-placenta and causing fetal asphyxia. This further provides strong evidence that good glycemic control before and during pregnancy may help improve pregnancy outcomes in pregnant women with diabetes. – – Translated from Cause of death in infants of women with pregestational diabetes mellitus and the relationship with glycemic control. Postgrad Med, 2009, 121:26 – 32.

Proximal small intestinal absence is thought to play an important role in the rapid improvement of metabolic regulation after diabetic gastric bypass. In this prospective randomized side-by-side cohort study, researchers evaluated and compared the effects of laparoscopic Roux-en-Y gastric bypass surgery (LRYGB) and laparoscopic cannula gastrectomy (LSG) on fasting and postprandial insulin, blood glucose, and glucagon-like peptide-1 (GLP-1) levels. The researchers randomized 13 patients to the laparoscopic Roux – en – Y gastric bypass group and another 14 patients to the laparoscopic cannula gastrectomy group. The majority of non-diabetic patients were evaluated before enrollment, 1 week and 3 months postoperatively. Patients in the two groups ate standard meals after fasting overnight, and blood samples were taken before and after meals to measure insulin, glucagon-like peptide-1, blood glucose, PYY and ghrelin levels, respectively. The results showed that the postoperative body mass and body mass index decreased significantly in both groups (P<0.02), with a similar decrease in body mass index at the third postoperative month. Postprandial plasma insulin and glucagon-like polypeptide-1 levels were significantly increased in both groups, and blood glucose metabolism improved. Compared with the laparoscopic cannula gastrectomy group, patients in the laparoscopic Roux-en-Y gastric bypass group experienced an increase in early phase insulin secretion at 1 week postoperatively, which may contribute to early postprandial glycemic control. There was no statistically significant difference in insulin and glucagon-like peptide-1 levels between the two groups at the third postoperative month. It can be seen that the above two operations can significantly improve the blood glucose level of patients; The findings do not support the idea that proximal small intestine resection can better improve blood sugar control. – – Translated from Improvement in glucose metabolism after bariatric surgery: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: a prospective randomized trial. Ann Surg, 2009, 250:234 – 241.