Volume 05 · Issue 04 · 2013

The changes of diabetes classification reflect the changes and progress of human understanding of diabetes. Initially, it was found that juvenile diabetes has different characteristics from adult diabetes, so diabetes is divided into juvenile and adult types, and it is divided into insulin-dependent and non-insulin-dependent diabetes according to whether insulin is needed to maintain life. The latest classification is based on the progress in the understanding of the pathogenesis of diabetes, which divides diabetes into four main types: type 1 diabetes, type 2 diabetes, special types of diabetes and gestational diabetes (GDM). In addition, there are some special manifestations in common types of diabetes, which also bring challenges to our clinical diagnosis and treatment. Strengthening the understanding of special types of diabetes and paying attention to distinguishing special manifestations in common types of diabetes are very important to improve the level of diabetes prevention and treatment.

On March 7, 2013, the "Yikai Cup" Diabetes Physician Salon of Chinese Diabetes Journal was successfully held in Beijing. This salon was hosted by Professor Ji Linong, Deputy Editor-in-Chief of Chinese Diabetes Journal, Department of Endocrinology, Peking University People's Hospital, and Director Yang Ying, Editorial Department of Chinese Diabetes Journal, and commented by Professor Guo Xiaohui, Department of Endocrinology, Peking University First Hospital. Dr. Zhou Xianghai from the Department of Endocrinology of Peking University People's Hospital and Dr. Gu Nan from the Department of Endocrinology of Peking University First Hospital reported two clinical cases respectively. More than 40 young and middle-aged doctors in the field of diabetes in Beijing, such as Peking Union Medical College Hospital, China-Japan Friendship Hospital of the Ministry of Health, Beijing Hospital, Chaoyang Hospital, Coal General Hospital, Fuxing Hospital and Guang' anmen Hospital of Traditional Chinese Medicine, participated in the discussion. "Yikai Cup" physician salon is co-organized by Changzhou Qianhong Pharmaceutical Co., Ltd.

maturity-onset diabetes of the young (MODY) is the most common monogenic diabetes, characterized by islet β cell dysfunction, accounting for about 1% to 2% of all diabetes mellitus, and is easily misdiagnosed as type 1 or type 2 diabetes. Since a definite diagnosis of MODY has an important impact on the treatment, prognosis and genetic counseling of patients, differential diagnosis should be actively performed. This article will briefly introduce the differentiation points of MODY from type 1 and type 2 diabetes, and the clinical characteristics of different subtypes of MODY.

The insulin gene encoding human insulin (INS) is located at 11p15.5, with a total length of 1355 bp and 3 exons. Exon 1 encodes a ribosome binding site on a mature mRNA, exon 2 encodes a start codon, a signal peptide, a B chain, and a C peptide, and exon 3 encodes an A chain. Normal insulin consists of 16 kinds of peptide chains A and B and 51 amino acids. Among them, the sulfhydryl groups in the four cysteines A7-B7 and A20-B19 form two disulfide bonds, which connect the A and B chains. In addition, there is also a disulfide bond between A6 and A11 in the A chain. In recent years, many studies have confirmed thatINSMutations are associated with the onset of special types of diabetes such as neonatal diabetes, adult-onset juvenile diabetes mellitus (MODY), idiopathic diabetes (Figure 1)^[1,2,3,4,5]。

To analyze gene mutation on KCNJ11 gene in 27 patients with infancy and early childhood diabetes mellitus.

Total of 27 patients(13 boys and 14 girls) diagnosed with infancy or early childhood diabetes mellitus on 30 days to 2 year and 7 months after birth and their parents were chosen as subjects. TIANamp blood DNA kit techniques were used to extract genomic DNA from peripheral white blood cells, polymerase chain reaction(PCR) techniques were used to amplify the KCNJ11 gene, after which DNA direct assay techniques were used to analyze gene mutation on KCNJ11.

A in-frame 15-bp KCNJ11 deletion was identified in a patient diagnosed with neonatal diabetes mellitus (c．82-96del), which resulted in 5 amine acids deletions (A28-R32), while no KCNJ11 deletions were found in her parents. The patient was responsive to the treatment of glibenclamide. A heterozygous c. 1096G>T (G366W) mutation was identified in a girl diagnosed with diabetes at 1 year and 7 months after birth, and her father carried the same mutation. NoKCNJ11 mutations were found in other paitents.

The rare c. 82-96del mutation on KCNJ11 can lead to neonatal diabetes mellitus.Also the mutation on KCNJ11 can lead to infancy and early childhood diabetes mellitus, while the onset mechanism is not clear.

To summarize the clinical characteristics, treatment response and follow-up data of Chinese permanent neonatal diabetes patients to improve clinical management.

A total of 30 permanent neonatal diabetes patients admitted to Peking Union Medical College Hospital from August, 2007 to August, 2012 were enrolled in this study. The clinical feature of onset, symptoms, signs, treatment response and follow-up data were analyzed.

Abnormal birth weight, including both small for gestational age (SGA) and macrosomia, was observed in 7(23.3%) cases. Ketosis was the manifestation at diagnosis in 25(83.3%) cases. Fasting C peptide and insulin levels were reduced in 19(63.3%) cases. Nerve system abnormalities were found in 5 cases(16.6%), including strength weakness, poor language function, epilepsy and central nerve system radiographic abnormalities, but with good prognosis. Abdominal malformation was found in 3 cases by ultrasound. A total of 4 cases had been successfully switched from insulin injection to oral glibenclamide. All cases were under good glycemic control without obvious adverse events.

Ketosis could be the first manifestation at diagnosis among most Chinese permanent neonatal diabetes patients, with reduced fasting C-peptide and insulin levels and sometimes with abnormalities in other systems. Most permanent neonatal diabetes patients should be treated with insulin, while oral glibenclamide could be efficacious in some patients.

To investigate the clinical characteristics, cause of disease and response to treatment on acquired partial lipodystrophy(APL).

From 1991 to 2012, 3 Chinese APL patients were studied.

3 patients of APL were all female, onset of disease were all around 10 years old, and the age of diagnosis were 20-62 years old. They were followed 2-12 years and now they are 25-65 years old. The subcutaneous adipose tissue was significantly decreased in upper body and was not affected or increased in the lower body in all 3 patients. Diabetes was diagnosed in all 3 patients and they were all with hyperinsulinemia, hypertriglyceridemia and fatty liver. Complement C₃ were lower than lower limit of normal in 2 patients. Two patients had normal menstruation, one patient had normal pregnancy. The 3 patients were treated on the basis of pioglitazone, blood glucose was well controlled and serum triglyceride decreased to normal, but the severely decreased subcutaneous adipose tissue in upper body didn't recover.

With treatment on the basis of pioglitazone, 3 APL patients can be well controlled metabolically, but the severely decreased subcutaneous adipose tissue in upper body couldn't recover.

To observe the plantar pressure distribution of type 2 diabetic patients in forward walking and backward walking, explore the significance of backwarding that may exit.

A total of 114 patients with type 2 diabetes (DM group, male 58, female 66 cases, age(53±11)yrs) were recruited from June 2011 to May 2012. Eighty-three healthy people (DC group, male 40, female 43 cases, age(51±13)yrs) were compared during the same period. The plantar pressure distribution was measured by foot peak pressure and impulse in the forward walking and backward walking. Two-sample t test was used for statistical analysis.

(1)Forward walking: compared with the control group, the peak foot pressure in the metatarsal 1, 3(M1, M3), heel medial(HM) were increased in the diabetic group. The highest pressure was at M3 (left foot: the control group (16.5±2.0) N/cm^2, diabetic group (21.9±5.0) N/cm^2; right foot: the control group (18.2±2.8) N/cm^2, diabetic group (19.4±4.4) N/cm^2, the difference was statistically significant(t=-10.46, -2.31, both P<0.05)). (2)Forward walking: compared with control group, the impulse increased in the toe 1(T1), metatarsal 1 to 5(M1 to M5), foot central arch or mid foot(MF), heel medial(HM) and heel lateral(HL)in diabetic group, especially in the M3 area (left foot: (50±11)N·s in the control group, (87±21)N·s in the diabetic group; right foot: the control group (62±15)N·s, diabetic group (84±19)N·s,t=-16.24, -8.60, both P<0.05). (3) Compared with forward walking, the peak pressure at T1, toe 2-5(T2-5), M1, MF, HM and HL had different degrees of increase in the diabetic patients with backward walking, but the peak pressure was significantly reduced in M3 (left foot were (22±5), (12±5) N/cm^2, right foot were (19±4), (15±6) N/cm² , t=15.10, 5.61, both P<0.05). (4)Compared with forward walking, the impulse was increased in T1 and T2-5 areas in the diabetic group with backward walking, especially in T1 zone(left foot: (54±18), (81±16) N·s, right foot: (29±11), (75±18) N·s ,t=-11.85, -23.90, both P<0.05); but the impulse at M2, M3, M4 was less than the same parts of impulse at the forward walking, especially in M3 zone(left foot: (87±21), (61±18) N·s, right foot: (84±19), (59±18) N·s,t=9.82, -9.63, both P<0.05).

Compared with normal subjects, the plantar peak pressure and impulse distribution in patients with diabetes are different. Backward walking may improves the plantar pressure distribution of diabetic patients.

To investigate the effect of sleep quality on glycemic control and relevant factors involved in subjects with type 2 diabetic mellitus(T2DM).

A total of 200 inpatients with T2DM were enrolled in this study. Each patient completed Pittsburg Sleep Quality Index (PSQI) questionnaire. The glycemic control target was <7%. All patients were evaluated by Zung Self-rating Depression Scale (SDS) for the mental status, the score of SDS ≥50 was defined as a depressive state. Patients were divided into two groups: non-sleep disorder group ( n=88) and sleep disorder group (n=112) according to PSQI score ≥7 which was defined as the sleep disorder. The clinical characteristics of two groups were compared and analyzed.

The incidence of sleep disorder was 56% in the overall population. In the sleep disorders group, Age, hemoglobin A, glycosylated (HbA1c), fasting plasma glucose, 0.5-hour as well as 2-hour postprandial plasma glucose, fasting serum total cholesterol, triglycerides, the score of SDS and the incidence of depression were significantly greater (t=-19.49--1.99, χ²=9.931, all P<0.05), whereas fasting C-peptide, 0.5-hour postprandial C-peptide and body mass index (BMI) were significantly lower (t=2.07, 2.14, 2.35, all P<0.05) than those of the non-sleep disorder group. Glycemic control target rate of PSQI<5 group, PSQI≥5 to 7 group, PSQI ≥7 to 9 group and PSQI≥9 group was 27.9%, 19.6%, 10.0% and 8.6%, respectively. Patients with a higher score of PSQI were less likely to reach glycemic targets (P< 0.05). Multiple logistic regression analysis indicated that sleep disorders was positively correlated with increased age, male, HbA1c and depression, however, sleep disorders was negatively related to BMI (OR=1.04, 2.38, 2.98, 2.14, 0.89, respectively, all P<0.05). There was a positive association between sleep disorders, 2-hour postprandial plasma glucose and HbA1c≥7%, however, HbA1c≥7% was inversely associated with insulin therapy (OR=2.81, 1.21, 0.33, all P<0.05).

Sleep disorders are prevalent in patients with T2DM. Hyperglycemia and sleep disorders interact with each other. Sleep disorders probably cause psychological health problems. Management of sleep quality and glucose control in patients with T2DM should be an effective approach for sleep and higher glycemic control target rate.

To investigate the prevalence of metabolism syndrome (MS) among adults in Guiyang urban areas and analyze its influencing factors.

Total of 1512 inhabitants aged twenty years and above living in a community of Guiyang urban areas were investigated from November 2009 to February 2010 by adopting stratified cluster sampling method (634 males and 878 females). The subjects were divided into six age groups (≥20-30, ≥30-40, ≥40-50, ≥50-60, ≥60-70 and ≥70 years). Questionnaires, physical examinations and determination of related metabolic index were carried out in the subjects. MS was defined according to global consensus of International Diabetes Federation (IDF) in 2005. Comparison of rate between groups was analyzed by the χ ² test, and comparison of mean values was statistically analyzed with t test.

The crude prevalence of MS among the investigated population was 29.7%, and it was higher in females than that in males(32.0% vs 26.5%, χ ²=5.346, P<0.05), and standardized MS prevalence was 29.1% (26.6% in male, 31.6% in female). The prevalence of MS increased with the increase of age, and it reached peak at ≥60-70 and ≥40-50 years in females and males, respectively. The crude prevalence of central obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol and increased blood pressure and fasting blood glucose among investigated population was 39.5%, 38.0%, 49.1%, 35.9% and 55.2%, respectively; and the standardized prevalence of above-mentioned indexes was 38.3%, 39.4%, 47.6%, 36.1% and 56.0%, respectively. In investigated population, 1335 (88.3%) had more than one metabolic component abnormality. Among MS patients, those who had 3, 4 and 5 metabolic component abnormalities accounted for 43.2%, 39.9% and 16.9%, respectively.

The prevalence of MS among adults in Zhaiji community of Guiyang urban areas is higher, so the prevention work of MS should be further strengthened.

To investigate the effect and mechanism of metformin on endothelial cell damages induced by intermittent high glucose.

Cultured human umbilical vein endothelial cells (HUVECs) were divided into six groups: normal glucose control, hyperosmotic control, constant high glucose, fluctuating high glucose, fluctuating high glucose + metformin and fluctuating high glucose + metformin + compound C. After incubation for 72 h, the level of nitric oxide (NO) production was shown as cell supernatant nitrite concentration which was measured by nitrate reductase method; the intracellular level of reactive oxygen species (ROS) was detected by flow cytometry; and the expression levels of adenosine monophosphate activated protein kinase (AMPK), phospho-AMPK (Thr-172, p-AMPK) and guanosine 5'-triphosphate cyclohydrolase-1 (GTPCH1) proteins were determined by western blot. One-way analysis of variance andQ test were applied to analyze the differences among the groups.

(1) Compared with those in the normal glucose control group (100%), the level of intracellular ROS ( (222±62)% ) was increased and the level of NO ( (70.3±7.1)% ) was reduced in the fluctuating high glucose group. The level of intracellular ROS ( (100±17)% ) was decreased and the level of NO ( (96.3±9.2) % ) was increased in the fluctuating high glucose group by adding metformin. The level of intracellular ROS ( (167.2±19.6)% ) was increased and the level of NO ( (83.3±8.7)% ) was decreased by further adding compound C, an AMPK inhibitor. All the differences were statistically significant (all P<0.05). (2) Compared with those in the normal glucose control group, the expression levels of p-AMPK ( (1.72±0.08) vs (2.34±0.09) ) and GTPCH1 ( (4.07±0.17) vs (7.83±0.56) ) were significantly downregulated in the fluctuating high glucose group. The expression levels of p-AMPK (2.72±0.22) and GTPCH1 (10.24±1.05) were increased in the fluctuating high glucose group by adding metformin. The expression level of GTPCH1 (2.39±0.34) was decreased by further adding compound C. All the differences were statistically significant (allP<0.05).

Metformin may attenuate intermittent high glucose-induced endothelial dysfunction via upregulating GTPCH1 expression mediated by activation of AMPK signaling pathway.

According to the 2010 Chinese Guidelines for the Prevention and Treatment of Type 2 Diabetes Mellitus, basal insulin or exenatide treatment can be initiated in patients who are not well treated with oral hypoglycemic drugs^[1]。 Insulin glargine is a long-acting human insulin analog that controls blood sugar smoothly. Exenatide is a synthetic polypeptide containing 39 amino acids. It is a glucagon-like peptide 1 (GLP-1) receptor agonist, which can promote insulin secretion and exert a hypoglycemic effect through a glucose-dependent mechanism. This study investigated the therapeutic effect of exenatide or insulin glargine and the effect on the serum inflammatory factor tumor necrosis factor alpha (TNF-alpha) in patients with type 2 diabetes mellitus with poor glycemic control by oral hypoglycemic drugs.

No previous history of diabetes, but abnormal glucose metabolism caused by definite pancreatic disease and meeting the diagnostic criteria of diabetes, this type of diabetes is called pancreatic diabetes. Pancreatic diabetes mellitus was listed in "special types of diabetes mellitus" in the 1999 WHO diabetes classification. Compared with type 1 and type 2 diabetes, pancreatic diabetes has its own unique insulin secretion and metabolism characteristics, and its clinical manifestations, complications and prognosis are also different from the former two, especially the risk of developing pancreatic cancer is greatly increased. Therefore, the early diagnosis, prevention and treatment of pancreatic diabetes should be attached great importance in clinical work. The author will review the research progress of pancreatic diabetes in recent years.

Diabetes is a systemic disease. At present, the prevalence of diabetes in China is about 9.7%, about 92.4 million people, and there are 150 million people at high risk of diabetes^[1]。 diabetic peripheral neuropathy (DPN) is a common complication of diabetes, and there is no effective treatment at present. Some patients have been amputated due to foot ulcers. Therefore, for such high-risk groups, diagnostic technologies that can accurately detect and quantify the disease have become particularly important, not only to detect the progression of the disease, but also to evaluate the clinical efficacy. The eye is the only organ in the human body that can directly observe nerve fibers, especially corneal confocal microscopy (CCM) can quantitatively analyze the parameters of corneal nerve fibers, and previous studies have shown that the changes of corneal nerve fibers in diabetic patients are correlated with the degree of peripheral neuropathy. Therefore, the pathological changes of diabetic peripheral neuropathy can be evaluated by observing the changes of corneal nerve fibers. Compared with traditional techniques, corneal confocal microscope-assisted diagnosis technology is convenient, non-invasive, and has strong patient compliance. It has outstanding advantages in evaluating the damage and repair of small nerve fibers. In this paper, the structural and morphological changes of corneal nerve fibers in diabetic patients were systematically reviewed by confocal corneal microscope, and the advantages and broad prospects of assessing diabetic peripheral neuropathy by confocal corneal microscope assisted diagnostic technology were prospected.

Most of the epidemiological studies on chronic diseases such as diabetes and hypertension in China are based on Han population, while the epidemiological research on chronic diseases such as hypertension and diabetes in She population is still blank. Our research group conducted a detailed and in-depth epidemiological study on chronic diseases such as diabetes in She population in Fujian from July 2007 to September 2009. The epidemiological investigation results of diabetes are summarized as follows.

Case 1, female, 27 years old, Han nationality, student. He was admitted to hospital in September 2010 with the main complaint of "dry mouth, poly-drinking for 2 years, sore throat and fever for 1 day". He has a history of diabetes for 2 years, and the first onset was "ketoacidosis". He has been seen in many hospitals and is likely to be diagnosed as type 1 diabetes. Irregular use of "Novolin 30R" to control blood glucose, fasting blood glucose was controlled at 10.5-16.5 mmol/L, and ketoacidosis occurred repeatedly. Among the relatives, his grandfather and uncle suffered from diabetes. Physical examination: Blood pressure: 100/56 mm Hg (1 mm Hg =0.133 kPa), conscious, no obvious abnormalities in heart, lungs, abdomen, etc. (not described because systemic pigmentation was not paid attention to). Emergency blood biochemical test report: blood glucose 46.01 mmol/L, urine ketone body 3+. Blood gas analysis returns: pH: 7.116, residual base: -25.00 mmol/L. Cardiac color ultrasound showed that the amplitude of interventricular septal motion was low and flat, and the left ventricular systolic function was suspected to be reduced. Return of chest CT findings: bilateral pleural effusion and atelectasis of lower lobes of both lungs. B-ultrasound showed blood stasis in the liver. No obvious abnormalities were found in the fundus of both eyes. Determination of urinary microalbumin 20.00 mg/L. Diagnosis: (1) Diabetes, diabetic ketoacidosis. (2) Viral myocarditis, cardiac insufficiency (cardiac function grade III), bilateral pleural effusion. Adenosine cyclic phosphate, coenzyme, metoprolol sustained-release tablets, potassium and magnesium aspartate injection, Shenfu injection, pedopril tablets and other treatments were given, and the symptoms were relieved and discharged. In November 2010, he was readmitted to hospital due to chest tightness, palpitations, asthma, facial and lower extremity edema. Physical examination: blood pressure: 90/56 mm Hg, conscious, and slightly cyanotic lips. There was no resistance in the neck, the heart rate was 102 beats/min, and the heart sounds were low and blunt. Mild depressed edema of both lower limbs. Post-admission tests: glycated hemoglobin (HbA1c): 8.90%, aspartate aminotransferase (AST): 92 U/L, alanine aminotransferase (ALT): 81 U/L. Cardiac color ultrasound showed slightly smaller inner diameter of ascending aorta, enlarged right atrium, moderate to severe tricuspid regurgitation, and reduced left ventricular systolic function. Diagnosis: (1) Diabetes; (2) viral myocarditis, cardiac function grade II; Right pleural effusion. After diuresis, nutrition of myocardium and extraction of pleural effusion, the patient still suffered from asthma and discomfort. In March 2011, the patient went to the doctor again due to asthma. Physical examination: diffuse bronzed pigmentation was seen on the skin of the whole body, with scattered speckled blue-gray distribution in the bottom layer, which was obvious on the face, neck, distal extension of limbs, and back of hand. No mucous membranes such as mouth and vulva were seen, and no liver palms and spider nevus were found. Assay: Iron metabolism showed: total iron binding capacity: 65.31 μ mol/L (reference value 45-75 μ mol/L), ferritin:>1500.0 μ g/L (23.9-336.2 μ g/L), serum iron: 54.2 μ mol/L (9-32 μ mol/L), blood routine: hemoglobin: 155 g/L; Fasting C-peptide: 0.08 μ g/L (0.78-3.68 μ g/L); Glutamate decarboxylase antibody (GADA): negative; Pathological examination of liver puncture: A large amount of hemosiderin was deposited in liver cells, which showed that many liver cells showed apoptotic changes, fibroplasia in the portal area, lymphocyte infiltration and a large amount of hemosiderin was deposited, and iron staining (+ + + +) was consistent with the morphological changes of hemochromatosis liver. Diagnosis: Primary hemochromatosis. After intermittent venous bleeding and iron removal, the patient did not have any discomfort such as asthma, and the skin pigmentation was significantly improved.

In the 1970s, Hirata et al.^[1]Spontaneous hypoglycemia with methimazole was first reported in patients with Graves' disease who had never used insulin, with high titers of insulin antibodies detected in the body. Subsequently, with the increasing number of reports of such cases, the concept of insulin autoimmune syndrome (IAS) was put forward, that is, in certain specific populations, exogenous factors, such as sulfhydryl-containing drugs, can induce the body to produce insulin antibodies. These antibodies bind to endogenous insulin to prevent the biological effects of insulin from being exerted. When these antibody-insulin complexes dissociate in a large amount in a short period of time, it can lead to a transient increase in free insulin level and hypoglycemic reaction. 1960, Harwood^[2]The case of a chronic insulin-using type 1 diabetic patient, who had to discontinue insulin for 23 d due to persistent severe hypoglycemia, with high titers of insulin-antibody complexes detected in the body is reported. Subsequently, cases of autoimmune hypoglycemia caused by exogenous human insulin have been reported rarely. Since 2005, similar cases have been reported in China^[3,4]。 We reported a case of autoimmune hypoglycemia caused by exogenous human insulin in 2005^[5]Three other confirmed or highly suspected patients have been found one after another, and the report is as follows.

Rabson-Mendenhall syndrome is an extremely rare clinical syndrome, which is caused by insulin receptor gene mutation. Clinical manifestations can be subcutaneous fat loss, acanthosis nigricans, genital enlargement, hirsutism, tooth dysplasia, special facial appearance, severe hyperinsulinemia, etc. Its incidence rate is extremely low, and only more than 10 cases have been reported in the literature so far. In order to improve the understanding of this disease, we summarized a case of Rabson-Mendenhall syndrome admitted to the Department of Endocrinology of Beijing Children's Hospital affiliated to Capital Medical University in September 2011, and reviewed the relevant literature in order to improve clinicians' understanding of Rabson-Mendenhall syndrome.

In the last 10 years, more and more patients have undergone bariatric surgery to treat morbid obesity. Bariatric surgery results in sustained weight loss by one or more of the following three mechanisms: reduction of gastric volume (gastric banding surgery, vertical band stomach, and sleeve gastrectomy), reduction of absorption surgery (reduction or non-reduction of gastric volume: Rouxen Y gastric bypass surgery, duodenal transposition, biliopancreatic shunt, and jejunoileal bypass), and surgery to alter enterogenic hormones that control energy metabolism (neuroendocrine control of energy metabolism) (Rouxen Y gastric bypass surgery, duodenal transposition, biliopancreatic shunt, jejunoileal bypass surgery, and sleeve gastrectomy). Although many studies have confirmed the effectiveness and durability of bariatric surgery, there is also increasing evidence that bariatric surgery can produce significant nutritional and metabolic disorders, especially negative effects on bone mineral metabolism.

Gastrojejunal bypass, while treating obesity, can also improve blood glucose and insulin levels in diabetic patients and relieve symptoms associated with diabetes. Obese people have high bone mineral density, but the effect of type 2 diabetes on bone mass and bone microstructure is unclear. To this end, the researchers evaluated the changes in bone microstructural properties and the volumetric parameter bone density (vBMD) and its relationship with hormone levels after gastrojejunal bypass treatment for diabetes mellitus.

Because of its health benefits, vitamin D is getting more and more attention. Vitamin D deficiency can lead to skeletal diseases such as rickets, chondrosis, osteopenia, osteoporosis, but new evidence suggests a possible link between vitamin D deficiency and cardiovascular disease (CVD), including myocardial infarction, coronary insufficiency, coronary calcification, carotid intima thickening, heart failure, peripheral arterial vascular disease (PAD), stroke, hypertension, lipid metabolism disorders, metabolic syndrome, impaired glucose metabolism, type 2 diabetes, and even involvement in the development of subclinical atherosclerosis. Vitamin D directly affects vascular endothelial cell function and atherosclerosis, or indirectly by affecting cardiovascular risk factors, but its exact mechanism is controversial.

The impairment of bone metabolism by estrogen reduction and type 2 diabetes is well defined, and the effects of both on bone metabolism may be partly due to the reduction of insulin receptor substrates 1, 2 (IRS-1, IRS-2) and insulin-like growth factor 1 (IGF-1) in bone. But whether estrogen reduction exacerbates the role of type 2 diabetes on bone metabolic damage remains unclear. Therefore, this study aimed to determine whether bone mineral density (BMD) in type 2 diabetic rats induced by a long-term high-fat and high-glucose diet plus low-dose streptozotocin (STZ) after ovariectomy is more significantly reduced than in simply ovariectomized rats or type 2 diabetic rats, and whether the expression of important molecules in the insulin signaling pathway (such as IRS-1, IRS-2, and IGF-1) in ovariectomized type 2 diabetic rats is significantly reduced.