Volume 05 · Issue 03 · 2013

Obesity is closely related to metabolic abnormalities, and it is also a susceptible factor to atherosclerosis, type 2 diabetes, cardiovascular diseases, tumors, non-alcoholic fatty liver disease and other diseases. However, the obese population is not a single group. Since the 1980s, research on obese subgroups has increased day by day, and the concept of metabolically healthy but obese (MHO) has emerged. The MHO subset is characterized by obesity but insulin sensitivity, and seems to have some metabolic protective mechanisms. It is significantly different from at-risk obese with abnormal metabolism in terms of body fat distribution, metabolism and inflammatory spectrum, and weight loss efficacy, so it should be treated differently in scientific research and clinical practice.

In recent years, more and more evidence has shown that chronic inflammation is closely related to metabolic diseases such as obesity, type 2 diabetes, atherosclerosis, etc. With the deepening of related research, researchers have found that chronic low-grade inflammatory response is the core point of metabolic syndrome. This inflammatory state is different from common conceptual inflammation, such as cholecystitis and pancreatitis. It is a subclinical process (or pro-inflammatory state) of chronic and low-grade inflammation mediated by the immune system, characterized by chronic and low-grade sustained elevation of various pro-inflammatory factors and inflammatory markers such as tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP)^[1]。 Clinically, it was also found that patients with ectopic fat deposition (such as fatty liver, fatty pancreas, etc.) had higher levels of plasma inflammatory factors than normal controls^[2,3]While some drugs clinically used to treat non-alcoholic fatty liver decrease inflammatory factor levels in the body while improving liver fat deposition^[4]。 By summarizing the results of recent studies on inflammation and ectopic fat deposition, this paper discusses the relationship between chronic low-grade inflammation and ectopic fat deposition, which will help us to have a better understanding of the mechanism of ectopic fat deposition.

Obesity is due to the imbalance of energy metabolism, energy intake is greater than consumption, which leads to excessive body fat deposition^[1]。 Obesity is an important risk factor for hypertension, type 2 diabetes, cardiovascular and cerebrovascular diseases, etc. It is not only related to abnormal fat metabolism, but also the main component and pathophysiological basis of metabolic syndrome^[2]。 With the development of social economy and the change of lifestyle, the incidence of obesity has increased significantly at home and abroad. According to statistics, the overweight rate of Chinese residents is 17.6%, and the obesity rate is 5.6%. The overweight and obese population has approached one quarter of the total population^[3]。 Controlling obesity and reducing body fat accumulation can reduce the risk and incidence of cardiovascular disease, and enhancing energy expenditure has become a promising intervention strategy for the treatment or prevention of obesity. In recent years, it has been discovered that the cold-sensitive channel transient receptor potential (TRP) channel family M8 receptor (TRPM8) may be a new target for obesity intervention. This paper will introduce the structure and function of TRPM8, its relationship with brown adipose tissue and its weight loss mechanism.

To investigate the clinical characteristics of metabolically healthy obese (MHO) individuals, and to explore the risk of MHO individuals on metabolic abnormal diseases.

A total of 4076 subjects were evaluated for routine health examination in People's Hospital of Hunan Province from April 2006 to January 2010, 2830 individuals were enrolled excluding those with missing data.Of the subjects, 1367 individuals were followed up during 1-3 years after. Data were collected of those individuals on the clinical and biochemistry parameters. Analysis of variance, χ² test, trend test and risk analysis were used for data analysis.

The prevalence of obesity was 39.58% (1120/2830), and MHO was 23.30% (261/1120) in obesity. The proportion of MHO in females was higher than that in males (31.22% vs 21.64%, χ ²=8.126, P<0.05). Parameters including systolic blood pressure(SBP), diastolic blood pressure(DBP), fasting blood glucose(FBG), triglyceride(TG), low density lipoprotein cholesterol(LDL-C), aspartatetransaminase(ALT), uric acid(UA) and white blood cell(WBC) count, were lower (while high density lipoprotein cholesterol(HDL-C) was higher) in MHO than those in obesity with metabolic syndrome (t value was between 2.036 and 20.985, all P<0.05), and higher (HDL-C was lower) than those in normal controls (t value was between 3.458 and 10.978, all P<0.05). Following up for 1 to 3 years, the incidence of metabolic abnormal diseases in normal controls was 17.6% (44/250), the incidence of metabolic abnormal diseases in MHO was 46.8% (51/109), the risk of metabolic abnormal diseases in MHO was significantly higher than that in normal controls (OR=4.117, 95%CI: 2.503-6.770; P<0.05).

MHO shows an intermediate clinical features between normal controls and obesity with MS. Over time, the risk of metabolic abnormal diseases in MHO was significantly increased.

To study the changes and mechanisms of the function of islet β cells after short term lipid infusion and its relation to mitochondrial oxidative stress.

Twenty four SD rats(weight 160-170 g, 8-week old) were randomly divided into 2 groups with random number table: free fat acid(FFA) group and normal saline(NS) group, which were infused with fat emulsion or saline respectively.Catheters were implanted under pentobarbital anesthesia in the right atrium via the jugular vein and the left carotid artery.A technique for a 48 h infusion in unrestrained rats was used for fat emulsion and heparin or saline infusion.The infusion period started on day 2 after surgery.After 48 h infusion, fasting serum insulin(INS), venous free fat acid were determined.The intravenous glucose tolerance test and islet cell perifusion were conducted to evaluate the function of islet β cell.The rats in the two groups were sacrificed, and the pancreatic islets were isolated and collected.The expression of insulin receptor substrate-1(IRS-1), insulin receptor substrate-2(IRS-2), uncoupling protein-2(UCP2)gene in islets were detected by real-time polymerase chain reaction (PCR). Student's t test was used for data analysis.

The serum FFA and insulin concentration of blood in FFA group were higher than those in NS group(insulin (25.2±2.3) vs (18.6±1.7)mU/L, t=7.9, P<0.05, FFA (1.39±0.18) vs(0.64±0.10)mmol/L,t=12.8, P<0.05). The glucose stimulated insulin secretion increased in the FFA group than in NS group ((137±24) vs (80±16) mU/L in vivo,t=6.8, P<0.05; (272±4) vs (227±4) mU/L in vitro,t=28.6, P<0.05). The gene expression of IRS-1 in islets was significantly increased by 29.3%±2.6%(t=2.2, P<0.05), and the mRNA expression of IRS-2, UCP-2 increased by 345.1%±4.7% and 228.4%±4.2% in FFA group than those in NS group(t=3.4, 3.0, all P<0.05).

Lipid infusion in short-term increases the secretion of insulin but it can also increase the gene expression of UCP-2, which can damage islet β cells.

To investigate the effect of peroxisome hyperplasia activated receptor γ(PPAR-γ) agonist(PGZ) on the differentiation and function of nonadrenergic primary brown adipose tissue cells in mice with high fat diet-induced obesity, and try to provide new treatment for obesity and type 2 diabetes.

Primary BAT cells were separated from high fat diet-induced C57BL/6J obesity(HFD) mice and cultured in DMEM culture medium.The primary BAT cells were divided into 10 culture dishes equally, and assigned as PGZ treatment group, and control group(treated with normal saline), 5 dishes each group. The effects of PGZ on BAT cells were assessed by quantitative real-time polymerase chain reaction(RT-PCR), Gene of BAT: uncoupling protein-1(UCP-1); elongase of very long chain fatty acids(ELOVL3); PPAR-γ co-activator-1α(PGC1-α); PPAR-γ co-activator-1β(PGC1-β); PRD1-BF-1-RIZ1 homologous domain containing protein-16(PRDM16); CCAAT/enhancer binding protein β( CEBP/β); adiponectin: adipocyte fatty acid-binding protein2(AP2); cytochrome c oxidase1(CYC1); mitochondrial transcription factor A(TFAM). Western blotting was used to assess the expression of UCP-1 protein; and Oil red O staining was applied to measure the adipogenesis function of BAT. The t test is used between two groups, ANOVA and LSD test is used between multiple groups.

The expression of mRNA associated with BAT chararcteristic genes(UCP-1、ELOVL3、PGC1-α、PGC1-β), lipogeneic genes(AP2), mitochondrial genes(CYC1、TFAM), and differential genes(PRDM16、CEBP/β) increased in PGZ treated group when compared with those in control group, the relative expression of the genes in the two groups were listed as following: UCP-1: 1100.0±612.0, 2.0±0.4; ELOVL3: 1461.0±617.0, 2.0±1.2; PGC1-α: 8.1±2.8, 2.0±1.1; PGC1-β: 8.3±2.8, 2.0±1.3; adiponectin: 2.6±0.8, 1.0±0.7; AP2: 5.1±2.2, 1.00±0.24; CYC1: 3.1±0.8, 1.0±0.4; TFAM: 1.2±0.4, 1.00±0.25; PRDM16: 4.8±2.6, 2.0±0.3; CEBP/β: 6×10⁸±5×10⁸, 2.0±0.6; t=2.45-5.22, all P<0.05; the expression of BAT functional protein UCP-1 assessed by Western blotting increased in PGZ treated group than that in control(1.24±0.25 vs 1.00±0.14,t=2.63, P<0.05); the function of BAT adipogenesis measured by oil red O test increased in PGZ treated group than that in control (1.2±0.2 vs 1.0±0.1,t=2.45, P<0.05).

PPAR-γ agonist-pioglitazone(PGZ) may promote the differentiation and function of brown adipocytes. This effect may be one of the reasons for PGZ improving metabolism.

To explore the effect of alimentary tract reconstruction after gastrectomy on blood glucose in patients with gastric cancer complicated with type 2 diabetes mellitus(T2DM).

The clinical data was retrospectively analyzed in 66 cases who received radical surgery for gastric cancer with T2DM from January 2008 to January 2012 in Changhai Hospital. These patients were divided into two groups according to different types of digestive tract reconstruction: Billroth Ⅰ(n=26, group A) and Billroth Ⅱ(n=40, group B). The preoperative clinical features, including the age, course of T2DM, body mass index(BMI), glycated hemoglobin A1c(HbA1c), insulin dosage, fasting plasma glucose (FPG) and 2-hour postprandial plasma glucose(2 h PG), were observed and compared between the two groups. And on the time of one week and three months after surgery, the FPG, 2 h PG were compared between the both two groups. The data were compared by using analysis of variance.

There was no statistical difference in FPG and 2 h PG before and after operation in group A (both P>0.05). The FPG and 2 h PG in group B decreased significantly one week and three months after operation when compared with those before operation (FPG: (7.0±0.6) vs (6.1±0.4) vs (10.2±1.0) mmol/L,F=4.25, P<0.05; 2 h PG: (8.8±0.1) vs (7.3±1.1) vs (11.4±1.8) mmol/L,F=3.87, P<0.05). Moreover, the FPG and 2 h PG in group B were all significantly lower than those in group B one week and three months after the operation (FPG at one week after surgery (7.0±0.6) vs(10.0±0.7) mmol/L ,t=5.35, P<0.05, and three months after operation (6.1±0.4) vs (9.8±0.7) mmol/L,t=4.78, P<0.05; 2 h PG at one week after surgery (8.8±0.1) vs (12.3±0.5) mmol/L,t=6.12, P<0.05, and three months after operation (7.3±1.1) vs (11.7±0.6) mmol/L,t=6.78, P<0.05).

The Billroth Ⅱ anastomosis reconstruction for distal gastrectomy brings remarkable effects on hyperglycemia in patients with gastric cancer and T2DM.

To explore the target of blood pressure control in elderly patients with type 2 diabetes and hypertension.

A total of 707 elderly patients (male/female: 324/383) with type 2 diabetes and hypertension between January 2008 and January 2011 were enrolled from Fujian Provincial Hospital. 235 patients were assigned into intensive systolic blood pressure (SBP) control group (130-139 mm Hg, 1 mm Hg=0.133 kPa), while 472 patients were assigned into non-intensive SBP control group(140-159 mm Hg). Both groups maintained their SBP level for at least 3 years. All of subjects underwent 12-lead electrocardiogram, and the voltage of R wave in lead aVL(RaVL) was used to estimate the risk of cardiovascular disease. Estimated glomerular filtration rate (eGFR) was estimated by Cockcroft-Gault formula for evaluation the renal function. Multivariate logistic regression analysis was used while RaVL≥0.57 mV and RaVL<0.57 mV as the dependent variable.

The level of RaVL in intensive SBP control group and non-intensive SBP control group was 0.55(0.50-0.59), 0.58(0.52-0.64) mV, respectively. The difference between the two groups was not statistically significant(F=0.235, P>0.05). The value of eGFR in intensive SBP control group and non-intensive SBP control group was 59.6(56.2-63.1), 55.6(53.2-58.0) ml/min, respectively. The difference was also not statistically significant(F=1.289, P>0.05). Multivariate logistic regression analysis showed that the risk of non-intensive SBP control group was not higher than intensive SBP control group(OR=0.927, 95%CI: 0.567-1.514, P>0.05).

SBP below 140 mm Hg may not reduce cardiovascular and chronic renal disease risk in elderly patients with type 2 diabetes and hypertension.

To study the expression of integrase interactor 1(INI1) gene in the arterial wall of diabetic foot rats and its molecular mechanism in the blood vessel endothelial cells.

The 8-week old male Sprague-Dawley rats were used. The rats were injected with streptozotocin(STZ) through caudal vein to establish diabetic rat models. Sixteen diabetic rats were randomly assigned to 2 groups(8 rats in each group): operation group received bilateral ligation while control group received sham operation. The expression of INI1 mRNA and protein in the arterial wall cells were evaluated by using reverse transcription polymerase chain reaction (RT-PCR) and Western blotting methods in the two groups. INI1 specific siRNA (INI1-siRNA) was synthesized and transfected into human umbilical blood vessel endothelial cell (HUVEC-12) while other 2 group of HUVEC-12 cells received siRNA transfection by non-related sequence and blank sequence. The HUVEC-12 cell migration, angiogenesis and the gene expression of intercellular adhesion molecule 1 (ICAM-1), metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase 1 (TIMP-1), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and angiopoietin-2 (Ang-2)before and after transfection were evaluated and compared among the three HUVEC cell groups by t test and analysis of variance.

The expression of INI1 mRNA and protein in the arterial wall of diabetic rats is much higher than those in the control group(mRNA: 0.83±0.07 vs 0.21±0.03, t=23.03, P<0.01; protein: 0.92±0.08 vs 0.31±0.03,t=20.19, P<0.01). Compared with lipoplast control group and non-related sequence group, the expression ofINI1 mRNA and protein in INI1-siRNA transfected group of HUVEC-12 cells was suppressed(mRNA: 0.26±0.01, 0.75±0.08, 0.80±0.07, respectively; F=36.49, P<0.01; protein: 0.11±0.02, 0.79±0.12, 0.82±0.14, respectively;F=24.17, P<0.01), while the cell migration capacity was improved afterINI1-siRNA transfection(66±5, 35±3, 37±5, respectively; F=19.39, P<0.01). Compared with the control groups, the mRNA and protein expression ofICMA-1, MMP-2, VEGF, bFGF and Ang-2 were significantly increased while the expression of TIMP-1 was reduced in INI1-siRNA transfected group(all P<0.05).

INI1 could significantly suppress the angiogenesis and endothelial migration of the vascular endothelium, and these effects might be implemented through the regulation of ICMA-1, MMP-2, VEGF, bFGF, Ang-2 and TIMP-1.

To explore the effects and mechanism of osteoprotegerin (OPG) on apoptosis of human umbilical vein endothelial cells (HUVECs) induced by palmitate acids (PA).

HUVECs were divided into three groups: normal control group (treated with 0.4% bovine serum albumin(BSA)) , PA group (treated with 0.4 mmol/L PA), OPG group(pretreated by OPG(50, 100, 200, 400 μg/L) for 24 h, then treated with 0.4 mmol/L PA). Cells in the 3 groups were cultured for 24 hours, then cell apoptosis was assessed by flow cytometry and Hoechst 33258 staining. HUVECs were divided into 5 groups: normal control group (treated with 0.4% BSA), PA group (treated with 0.4 mmol/L PA), OPG group (pretreated by 400 μg/L OPG for 24 h, then treated with 0.4 mmol/L PA), PA+ OPG+ rapamycin group(pretreated with 10 μg/L rapamycin for 24 h, then treated with 400 μg/L OPG for 24 h, and then treated with 0.4 mmol/L PA), PA+ rapamycin group(pretreated with 10 μg/L rapamycin for 24 h, then treated with 0.4 mmol/L PA). The expression levels of tuberin, phosphorylated tuberin(P-tuberin), S6K, phosphorylated S6K(P-S6K), Bcl-2, Bax and caspase 3 protein were measured by western blotting analysis using specific antibodies. The data were compared among groups by using ANOVA followed by SNK test.

Compared with normal control group, the early apoptosis rate of HUVECs in PA group was significantly increased (18.31%±0.51% vs 6.88%±0.60%, P<0.05). And the early apoptosis of HUVECs decreased dramatically in OPG group compared with that in PA group (12.58%±0.19%, 9.39%±0.42%, 7.55%±0.17%, 5.90%±0.14%, respectively, allP<0.05) and in a OPG dose dependent manner. Compared with normal control group, the late apoptosis rate of HUVECs increased significantly in PA group (9.55%±0.22% vs 5.28%±0.90%,P<0.05). The late apoptosis of HUVECs decreased dramatically in OPG group compared with that in PA group(7.71%±0.17%, 6.42%±0.18%, 5.24%±0.16%, 4.50%±0.16%, respectively, allP<0.05) and in a OPG dose dependent manner. Compared with normal control group, the expression of P-tuberin/tuberin(2.094 2±0.0163 vs 1.1948±0.0541), P-S6K/S6K(2.0942±0.0163 vs 3.2052±0.0051), Bax/β-actin(0.3868±0.0013 vs 1.2991±0.0026), caspase 3/β-actin(0.2346±0.0009 vs 0.5793±0.0103) increased markedly in PA group (allP<0.05), Bcl-2/β-actin(0.2470±0.0038 vs 0.0716±0.0004)decreased significantly in PA group(P<0.05); Compared with PA group, the expression levels of P-tuberin/tuberin(0.8258±0.0074), P-S6K/S6K(2.5073±0.1403), Bax/β-actin(0.7452±0.0045), caspase 3/β-actin(0.4713±0.0066) in OPG group were significantly lower than those in PA group(allP<0.05), Bcl-2/β-actin(0.1909±0.0021)was significantly higher than that in PA group(P<0.05).

It suggests that protective effect of OPG on HUVECs cultured with PA may be association with tuberin/mTORC1 pathway.

To establish a repeatable and feasible method for culturing human glomerular podocytes in vitro.

The renal epithelial tissues were obtained from the tumor-free pole of adults' kidneys after kidney tumor resection. Decapsulated human cortical slices were pressed through a series of stainless steel sieves (sieving method) with increasing pore sizes of 220 to 450 μm in a sterile, clean environment; as a final step, the glomeruli were collected on a 125 μm sieve and then cultured in 25 cm² flasks of which bottoms were soaked by RPMI 1640 medium with 10% fetal bovine serum (FBS) in advance. Made the flasks upside down (explant method); 4 hours later, added medium and normally placed them. Cells were kept at 37 ℃ in a humid atmosphere under 5% CO₂. Glomerular podocytes cellular markers as nephrin, Wilms tumor protein(WT-1), factor Ⅷ, vimentin and cytokeratin were analyzed by morphology and indirect immunofluorescence staining method, respectively. The purity of podocytes were determine by flow cytometry technology.

Most of the glomeruli adhered to the wall of culture dish on the 3 rd day. Almost all glomeruli adhered on the 5 th day with a few climbed out polygonal cells which lost both primary and foot processes and appeared as cobblestones. A larger number of cobblestone-like cells which exhibited strong proliferative activity outgrowth from nearly every glomerular around from 7 th to 10 th day. Then the cells were digested by trypsin differences digestion method to remove fibroblast and subcultured. In subculturing, podocytes differentiate into other phenotypes which were large, branched, binucleated and exhibited no proliferative activity. It was observed by immunofluorescent staining that the cells were in line with characteristics of podocytes and expressed WT-1 and nephrin, but not the factor Ⅷ, vimentin and cytokeratin with no pollution of endothelial cells, mesangial cells and parietal epithelial cells. Furthermore, purity of podocytes was 98.3% checked by flow cytometry analysis.

It is simple and highly effective to culture primary cultured glomerular podocytes by combined sieving and explant method.

Diabetes mellitus is a chronic disease that seriously affects human health. Its morbidity and mortality are increasing, and the cost of medical care is rising year by year. It is rapidly becoming a global epidemic. By 2030, the number of people with diabetes worldwide will rise from 1.71 billion in 2000 to 3.66 billion^[1]。 The increasing incidence and prevalence highlights the need for innovation in diabetes management and prevention approaches. More and more studies have shown that vitamin D not only participates in traditional calcium and phosphorus metabolism, but also has a wide range of biological effects, such as inhibiting the proliferation of tumors and normal cells, inhibiting the production of inflammatory factors, regulating cell adhesion, regulating immune response, affecting the function of pancreatic islet β cells, affecting the synthesis and secretion of insulin and its peripheral effects, etc. The protective effect of vitamin D on pancreatic islet β cells and its mechanism are reviewed.

Diabetes is generally treated with oral medications and/or insulin based on lifestyle interventions. Novel hypoglycemic drugs based on glucagon-like peptide 1 (GLP-1) have achieved good efficacy in the clinical treatment of patients with type 2 diabetes^[1]。 GLP-1 is an incretin mainly produced by intestinal L cells, which exerts biological effects mediated by specific GLP-1 receptors (GLP-1R^[2]。 GLP-1R belongs to the glucagon receptor subfamily in the G protein-coupled receptor B family (secretin family), and is expressed not only in the pancreas, but also in extrapancreatic tissues, including central nervous system, gastrointestinal tract, cardiovascular, lung, kidney, lymphocytes, mesenchymal stem cells and other tissues^[3,4]。 The expression of GLP-1R and its physiological functions will be reviewed.

The activity of the cardiovascular system is regulated by the autonomic nervous system of the heart. When normal people move during the day and in standing position, the sympathetic nerve tension of the heart increases relatively, the heart rate increases, the myocardial contractility increases, and the conduction accelerates. At night and in lying rest, the activity of the parasympathetic nerves of the heart prevails, thus causing cardiac activity with physiological effects opposite to the excitation of the cardiac sympathetic nerves^[1], in patients with diabetic cardiovascular autonomic neuropathy, the autonomic nervous system that innervates the heart and blood vessels is imbalanced, mainly manifested by the loss of dominance of parasympathetic activity at night, thereby impairing the normal electrophysiological activity of the heart, resulting in heart rate and hemodynamic abnormalities^[2]。 Abnormal cardiac electrophysiological activity CAN be manifested as abnormalities of electrocardiogram parameters related to it, such as prolonged QTc interval, decreased heart rate variability and increased spatial QRS-T angle. Therefore, early recognition of these changes in electrocardiogram parameters CAN detect diabetic CAN early, which is of great significance to reduce the occurrence of cardiac accidents in diabetic patients. The relationship between electrocardiogram parameters and CAN at home and abroad in recent years is reviewed.

Alstrom syndrome (AS), also known AS obesity-retinal degeneration-diabetes syndrome, is a rare autosomal recessive genetic disease, which was first reported by Alstrom et al. in 1959^[1]So far, only more than 300 cases have been reported worldwide, and 5 cases have been reported in China^[2,3,4,5,6]。

Vitamin D is an important regulator of bone metabolism. Previous studies on the relationship between vitamin D deficiency and osteoporotic fracture are still controversial. Some prospective cohort studies have shown that serum levels of 25-hydroxyvitamin D [25- (OH) D] in the elderly are associated with osteoporotic fractures. However, the correlation between serum levels of 25- (OH) D and vertebral fractures in diabetic patients is not clear at present.

Type 2 diabetes is characterized by insulin resistance in various insulin target cells, and osteoblasts are insulin target cells involved in regulating the stability of glucose throughout the body. This new understanding suggests that weakened insulin signal transduction in osteoblasts may have an impact on the development of type 2 diabetes.

Recently, scholars have begun to pay attention to the relationship between osteocalcin and glucose metabolism. It has been reported that the skeletal system also plays a role in the regulation of sugar metabolism. In children, the association between lipid metabolism, adiponectin, and metabolic syndrome is well known, but the relationship between obesity, insulin resistance, and osteocalcin has not been proven. The aim of this study was to evaluate the prevalence of insulin resistance in obese children and adolescents, to explore the effects of adiponectin and osteocalcin on metabolic syndrome and insulin resistance and the association between osteocalcin, insulin resistance and adiponectin. To this end, the researchers included 150 obese non-diabetic children and adolescents aged 5 to 18 years in the study. The serum levels of adiponectin, osteocalcin and insulin were measured, and the relationship between the components of metabolic syndrome and the levels of adiponectin and osteocalcin was investigated.

In recent years, the relationship between gastrointestinal hormones and bone metabolism in diabetes has attracted increasing attention. This article gathers the results of in vitro and in vivo studies and systematic reviews to explore the in vitro effects of incretin drugs on osteoblasts and osteoclasts, and their effects on bone turnover rate and fracture risk in diabetic patients.