Functional Analysis of the Chemosensory Protein GmolCSP8 From the Oriental Fruit Moth, Grapholita molesta (Busck) (Lepidoptera: Tortricidae).

Chemosensory proteins (CSPs) belong to a family of small water-soluble proteins that can selectively bind and transport odorant molecules for olfactory communication in insects. To date, their definite physiological functions in olfaction remain controversial when compared with odorant binding proteins (OBPs). To investigate the functions of CSPs in the oriental fruit moth Grapholita molesta, we determined the tissue expression patterns and binding properties of the CSP, GmolCSP8. The key binding sites of GmolCSP8 with a representative ligand were evaluated using molecular flexible docking, site-directed mutagenesis and ligand-binding experiments. Multiple sequence alignment and phylogenetic analysis showed that GmolCSP8 possesses a typical conserved four cysteines motif and shares high sequence identity with some CSP members of other Lepidopteran insects. GmolCSP8 was predominantly expressed in the wings and antennae of both male and female adults and may be involve in contact chemoreception. Recombinant GmolCSP8 (rGmolCSP8) exhibited specific-binding affinities to small aliphatic alcohols (C4-12) and had the strongest binding affinity to 1-hexanol. The three-dimensional structure of GmolCSP8 was constructed using the structure of sgCSP4 as a template. Site-directed mutagenesis and ligand-binding experiments confirmed that Thr27 is the key binding site in GmolCSP8 for 1-hexanol binding, because this residue can form hydrogen bond with the oxygen atom of the hydroxyl group in 1-hexanol, and Leu30 may play an important role in binding to 1-hexanol. We found that pH significantly affected the binding affinities of rGmolCSP8 to ligand, revealing that ligand-binding and -release by this protein is related to a pH-dependent conformational transition. Based on these results, we infer that GmolCSP8 may participate in the recognition and transportation of 1-hexanol and other small aliphatic alcohols.

Clinical application of a novel diagnostic scheme including pancreatic ß­cell dysfunction for traumatic multiple organ dysfunction syndrome.

A novel diagnostic scheme that includes pancreatic ß­cell dysfunction analysis for the diagnosis of traumatic multiple organ dysfunction syndrome (MODS) was investigated to assist in the early diagnosis and detection of MODS. Early intervention and treatment of MODS has been associated with a reduced mortality rate. A total of 2,876 trauma patients (including patients post­major surgery) were admitted to the intensive care unit of the authors' hospital between December 2010 and December 2015 and enrolled in the present study. There were 205 cases where the patient succumbed to their injuries. In addition to the conventional diagnostic scheme for traumatic MODS, indexes of pancreatic ß­cell dysfunction [fasting blood­glucose (FBG), homeostatic model assessment­ß and (blood insulin concentration 30 min following glucose loading­fasting insulin concentration)/(blood glucose concentration 30 min following glucose loading­FBG concentration)] were included to establish an improved diagnostic scheme for traumatic MODS. The novel scheme was subsequently used in clinical practice alongside the conventional scheme and its effect was evaluated. The novel scheme had a significantly higher positive number of MODS diagnoses for all trauma patients compared with the conventional scheme (12.48 vs. 8.87%; P<0.01). No significant difference was identified in the final percentage of positive of MODS diagnoses for trauma­associated mortality patients between the novel (88.30%) and the conventional scheme (86.34%). The novel scheme had a significantly higher positive number of MODS diagnoses for trauma­associated mortality patients 3 days prior to patients succumbing to MODS compared with the conventional scheme (80.98 vs. 64.39%; P<0.01). The consensus of the MODS diagnosis of all trauma patients between the novel scheme and the conventional scheme was 100%; however, out of the patients diagnosed as positive by novel scheme 71.03% were positive by the conventional scheme. The consensus between the final MODS diagnosis and the MODS diagnosis 3 days prior to patients succumbing to their injuries between the novel scheme and the conventional scheme was 100%; however, out of the patients diagnosed as positive by novel scheme 97.79 were positive by the conventional scheme of the 205 patients who succumbed to MODS and out of the patients diagnosed as positive for MODS by novel scheme 3 days prior to succumbing, 79.52% were positive by the conventional scheme. The results of the present study demonstrated that the novel diagnostic scheme using the relevant indexes of pancreatic ß­cell dysfunction for diagnosis of traumatic MODS, was able to diagnose MODS early without excessively extending the diagnostic scope. Its clinical application should be promoted.

Glucotoxicity and α cell dysfunction: involvement of the PI3K/Akt pathway in glucose-induced insulin resistance in rat islets and clonal αTC1-6 cells.

AIM/HYPOTHESIS: The objective of this study was to assess how long-term exposure to high glucose affects the α cell function and whether the increased glucagon secretion is mediated via insulin resistance. MATERIALS AND METHODS: We established a ß cell-depleted rat model to obtain pure primary α cells. Furthermore, isolated rat islets and TC1-6 cells (a clonal α cell line) were exposed to high glucose (25 or 30 mmol/L) and low glucose (5.5 mmol/L) for up to 5 days to evaluate the influence of chronic glucose toxicity on glucagon secretion and glucagon gene expression. Moreover, we added insulin and/or Wortmannin to examine if the inhibitory effect of insulin on glucagon secretion was impaired by high glucose via the phosphatidylinositol 3 kinase/PKB protein kinase B pathway. RESULTS: Both glucagon secretion and glucagon gene expression were increased in response to 5 days exposure to high glucose. While a moderate insulin concentration slightly inhibits glucagon secretion from rat islets and α TC1-6 cells at high glucose, a pronounced increase in glucagon secretion was observed at low glucose. We found that the insulin-mediated activity of the phosphatidylinositol 3 kinase/PKB protein kinase B pathway in the α cell was markedly impaired by chronic exposure to high glucose. CONCLUSION: The hypersecretion of glucagon induced by glucotoxicity may be secondary to insulin resistance of the α cell induced by impaired activity of the insulin signaling pathway.

Involvement of calcium-sensing receptor in oxLDL-induced MMP-2 production in vascular smooth muscle cells via PI3K/Akt pathway.

Matrix metalloproteinase-2 (MMP-2) is constitutively expressed in vascular smooth muscle cells (VSMCs) and up-regulated in atherosclerotic lesion by various stimuli, such as oxidized low-density lipoprotein (oxLDL). Calcium-sensing receptor (CaSR) is also expressed in VSMCs, but it remains unclear whether CaSR is associated with overproduction of MMP-2 in VSMCs. In this study, the expression of MMP-2 was detected by real-time PCR and Western blot analysis, and the gelatinolytic activity of MMP-2 was measured using gelatin zymography. Our results showed that oxLDL enhanced MMP-2 expression and activity in rat aortic VSMCs in a time- and dose-dependent manner. In addition, CaSR expression was up-regulated by oxLDL. Manipulating CaSR function in these cells by NPS2390 (an antagonist of CaSR) or GdCl(3) (an agonist of CaSR) affected the oxLDL-induced MMP-2 production. In VSMCs, oxLDL stimulated the rapid activation of phosphatidylinositol 3-kinase (PI3K)/Akt signal pathway, as determined by Western blot analysis. Phosphorylation of Akt and MMP-2 production stimulated by oxLDL were attenuated by LY294002 (a specific inhibitor of PI3K). Activation of Akt was suppressed by NPS2390 but enhanced by GdCl(3). In contrast, oxLDL had no stimulatory effect on the phosphorylation of JNK, and pretreatment with SP600125 (an inhibitor of JNK) produced no significant effect on oxLDL-induced MMP-2 production. These results suggest that CaSR mediates oxLDL-induced MMP-2 production in VSMCs via PI3K/Akt signal pathway.

Calcium-sensing receptors induce apoptosis during simulated ischaemia-reperfusion in Buffalo rat liver cells.

1. Calcium-sensing receptors (CaSR) exist in a variety of tissues. In 2010, we first identified its functional expression in Buffalo rat liver (BRL) cells and demonstrated that the activation of CaSR was involved in an increased intracellular calcium through the Gq subunit-phospholipase C-inositol triphosphate pathway. However, its role and related mechanism in hepatic ischaemia/reperfusion (I/R) injury is still unclear. 2. Therefore, in the present study, BRL cells were incubated in ischaemia-mimetic solution for 4 h, then reincubated in the normal culture medium for 10 h to establish a simulated I/R model. We assayed the apoptotic ratio of BRL cells by flow cytometry and Hoechst 33342 staining; analyzed the expression of CaSR, cytochrome c (Cyt-c), caspase-3, Bcl-2, Bax, extracellular signal-regulated protein kinase (ERK), and p38 by Western blotting; and measured the concentration of intracellular calcium by laser-scanning confocal microscopy. 3. The results showed that simulated I/R increased the expression of CaSR and induced apoptosis in BRL cells. GdCl(3), a specific activator of CaSR, further increased CaSR expression, intracellular calcium, and apoptosis in BRL cells during I/R. The activation of CaSR downregulated Bcl-2 expression, upregulated Cyt-c, caspase-3, and Bax expressions, and promoted p38 and ERK-1/2 phosphorylation. 4. In conclusion, increased CaSR expression plays a vital role in apoptosis induced by I/R injury, in which its mechanism is related with calcium overload and the activation of the mitochondrial and mitogen-activated protein kinase apoptotic pathways. The regulation of CaSR activity might serve as a novel pharmacological target to prevent and treat liver disease.

The calcium-sensing receptor mediates hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells through MEK1/ERK1,2 and PI3K pathways.

Activation of the calcium-sensing receptor (CaSR) leads to an increase of intracellular calcium concentration and alteration of cellular activities. High level of intracellular calcium is involved in hypoxia-induced proliferation of pulmonary arterial smooth muscle cells (PASMCs). However, whether the CaSR is expressed in PAMSCs and is related to the hypoxia-induced proliferation of PASMCs is unclear. In this study, the expression and distribution of CaSRs were detected by RT-PCR, western blotting and immunofluorescence; the intracellular concentration of free calcium ([Ca(2+) ](i) ) was determined by confocal laser scanning microscopy; cell proliferation was tested using an MTT and BrdU incorporation assay; cell cycle analysis was carried out using a flow cytometric assay; and the expression of proliferating cell nuclear antigen (PCNA), extracellular signal-regulated protein kinase 1,2 (ERK1,2) and AKT were analysed by western blotting. We observed that both CaSR mRNA and protein were expressed in rat PASMCs. Lowering of oxygen from 21% to 2.5% led to increased [Ca(2+) ](i) and CaSR expression. This condition of hypoxia also stimulated PASMCs proliferation accompanying with increased phosphorylation of ERK1,2 and AKT. GdCl(3) (an agonist of CaSR) or NPS2390 (an antagonist of CaSR) amplified or weakened the effect of hypoxia, respectively. PD98059 (a MEK1 inhibitor) or LY294002 (a PI3K inhibitors) decreased the up-regulation of PCNA expression and the increase of the cell proliferation index induced by hypoxia and GdCl(3) in PASMCs. Our results suggest that CaSR is expressed in rat PASMCs, and that CaSR activation through MEK1/ERK1,2 and PI3 kinase pathways is involved in hypoxia-induced proliferation of PASMCs.

Downregulation of the ornithine decarboxylase/polyamine system inhibits angiotensin-induced hypertrophy of cardiomyocytes through the NO/cGMP-dependent protein kinase type-I pathway.

BACKGROUND: Polyamines and nitric oxide (NO) have been involved in the pathogenesis of cardiac hypertrophy. NO can regulate cardiac ion channels by direct actions on G-proteins and adenyl cyclase. The present study was undertaken to elucidate the molecular mechanism of interactions with polyamines and NO in cardiac hypertrophy. METHODS: Cardiaomyocyte hypertrophy was induced by angiotensinII (AngII). Hypertrophy was estimated by cell-surface area, atrial natriuretic peptide (ANP) mRNA expression, and the immunofluorescence of phalloidin. Pretreatment with alpha-difluoromethylornithine (DFMO) was done to deplete putrescine; KT5823 pretreatment was carried out to block the nitric oxide/cGMP-dependent protein kinase type-I (NO/PKG-I) pathway. Expressions of endothelial nitric oxide synthase (eNOS), PKG-I, c-fos and c-myc were analyzed by western blotting and immunofluorescence. The intracellular concentration of free calcium ([Ca2+](i)) was determined by confocal laser scanning microscopy. RESULTS: Hypertrophy of cardiomyocytes was induced by AngII, this caused an increase in putrescine, spermidine and total polyamine pool in association with a decreased level of NO. Expressions of eNOS and PKG-I were down-regulated, [Ca2+](i) was increased, and expressions of c-Fos and c-Myc upregulated. DFMO reversed these changes induced by AngII. CONCLUSIONS: Downregulation of polyamines inhibits cardiomyocyte hypertrophy, which is closely related to [Ca2+](i) and the NO/PKG-I pathway.

[Impact of metabolic syndrome with hyperglycemia on prevalence of stroke in Chinese].

OBJECTIVE: To investigate the impact of metabolic syndrome (MS) with or without hyperglycemia on stroke prevalence compared to that of diabetes alone. METHODS: 44 100 subjects, 20 570 males and 23 530 females, aged 25 - 75, who had participated in the Chinese Residents Nutrition and Health Examination Survey held in the mainland of China 2002, underwent anthropometry, measurement of total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), high density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), and 2 hour plasma glucose (2 h PG) after 75 g oral glucose tolerance test (OGTT). 22 570 subjects, 10 698 males and 11 872 females, were divided into 5 groups: control group without MS risk factors (n = 17 518), Group of diabetes mellitus (DM) without MS (n = 638), group of MS with normoglycemia (n = 2501), Group of MS with mild hyperglycemia (n = 1058), and group MS with DM (n = 855). The relationship between MS and stroke was studied by multiple logistic regression analysis. RESULTS: The prevalence of MS increased along with age. The MS prevalence rates of the subjects with FPG > or = 5.6 mmol/L in the age groups 25 - 34, 35 - 44, 45 - 54, and > or = 55 were 23.5%, 37.2%, 45.7%, and 53.0% respectively, all significantly higher than those of the subjects with the FPG < 5.6 mmol/L (2.2%, 4.7%, 7.8%, and 9.5% respectively, all P < 0.01). The prevalence rates of stroke of the groups of DM, normal blood sugar with MS, mild hyperglycemia with MS, and DM with MS were 2.94%, 2.27%, 2.89%, and 4.11%, respectively, all significantly higher than that of the control group (0.19%, all P < 0.01). After adjustment for age, sex, smoking status, and LDL-C, no significant difference was observed between the neighboring MS groups (all P > 0.05). Compared to the group of MS with normoglycemia, the OR value for stroke of the DM with MS was 1.84 (95% CI 1.20 - 2.83, P < 0.01), which was still significant after adjusting for LDL-C (P < 0.05). CONCLUSION: (1) People with glucose intolerance had very high prevalence of stroke than novmoglgcemic people. (2) Hyperglycemia in MS has an extremely important role in the impact of MS on stroke in Chinese. (3) Diabetes by itself has the same significance as the combination of MS components in the development of stroke.

[The association of stroke with high plasma low-density lipoprotein cholesterol level and metabolic syndrome in Chinese adults].

OBJECTIVE: To investigate the impact of high plasma LDL-C level with or without metabolic syndrome (MS) on the incidence of stroke in Chinese adults. METHODS: Totally 42 626 subjects (25-75 years old) from Chinese National Health and Nutrition Survey in 2002 were stratified four groups based on plasma LDL-C level:<2.00 mmol/L group, 2.00-2.50 mmol/L group, 2.51-3.31 mmol/L group, and >or=3.32 mmol/L group. The prevalence of MS (with 2005 International Diabetes Federation criteria) and stroke and the risk factors of stroke were compared among the four groups. RESULTS: (1) The prevalence of MS and stroke increased with rising of LDL-C level. The prevalence of MS in LDL-C>or=3.32 mmol/L group increased 2.5 times (7.9% vs 20.1%) as compared with that in LDL-C<2.00 mmol/L group and the prevalence of stroke increased 4.2 times (0.5% vs 2.1%), all P<0.01. (2) In subjects with similar LDL-C level, the prevalence of stroke was significantly higher in a subgroup with MS than that without (P<0.01). (3) After adjustment for age, sex and smoking, logistic regression analysis showed that both LDL-C level and MS were positively associated with the development of stroke; the odds ratio (OR) was 2.35 and 3.15 (P<0.0001), respectively. (4) Compared with the subgroup of LDL-C<2.00 mmol/L without MS, OR for stroke in the subgroups of LDL-C 2.00-2.50 mmol/L, 2.51-3.31 mmol/L, and >or=3.32 mmol/L without MS was 1.03, 1.89, and 2.08, whereas the OR for stroke in the subgroups with MS and similar level of LDL-C was 4.38, 5.23 and 6.15; this indicated that the risk of stroke in subjects with MS increased by 3-4 times compared with subjects without (P<0.0001). CONCLUSION: Both high LDL-C level and MS are independent risk factors of stroke, but the risk of stroke will be further increased in the presence of high LDL-C level plus MS. It is suggested that combined intervention therapy of LDL-C and MS will play an important role in the prevention of stroke.

[The role of syntaxin1A/synaptosome-associated protein-25 in reversing hyperglycemia-induced alpha cell toxicity].

OBJECTIVE: To investigate the effects of reversal of hyperglycemic toxicity on the synthesis and secretion of glucagon by the alpha cells and the possible mechanisms thereof. METHODS: Mouse glucagonoma cells of the line TC1-6 were cultured in medium containing 5.5 mmol/L glucose for 10 days (low glucose group, LG), in medium containing 25 mmol/L glucose for 10 days (high glucose group, HG), in medium with 25 mmol/L glucose for 5 days and then in medium with 5.5 mmol/L glucose for 5 days (high-low glucose group, HL group), or in medium with 5.5 mmol/L glucose for 5 days and then in medium with 25 mmol/L glucose for 5 days (LH group), Radioimmunoassay was used to detect the glucagon concentration in the supernatant. RT-PCR was used to detect the mRNA expression of glucagon in the TC1-6 cells. Western blotting was used to detect the protein expression of the Snare proteins: syntaxin1A and synaptosome-associated protein (SNAP)-25. RESULTS: (1) The glucagon level of the HG/LG group was lower than that of the HG group by 29% (P < 0.05). (2) The glucagon mRNA expression level in the TC1-6 cells of the HG/HL group was significantly lower than that of the HG group by (52.6 +/- 2.8)% (P < 0.05). (3) The syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG group were significantly higher than those of the LG group by 36% and 69% respectively (both P < 0.05), and the syntaxin1A and SNAP-25 expression levels in the TC1-6 cells of the HG/LG group were significantly lower than those of the HG group by 49% and 56% respectively (both P < 0.05). CONCLUSION: After removing the high glucose toxicity the abnormal glucagon secretion by the alpha-cells can be ameliorated obviously, and the expression levels of syntaxin1A and SNAP-25 proteins that promote the secretion of glucagon are reduced accordingly.

[Impairment of pancreatic islet beta cell function induced by intermittent high glucose through oxidative and endoplasmic reticulum stress: experiment with rat pancreatic islet beta cells].

OBJECTIVE: To investigate the effect of intermittent high glucose (IHG) on the pancreatic islet beta-cell function and mechanism thereof. METHODS: Rat pancreatic islet p-cells of the line INS-1 were cultured and randomly divided into 3 groups: IHG group exposed to fluctuating concentrations of glucose, stable high glucose (SHG) group exposed to 16. 7 mmol/L glucose, and control group exposed to normal concentration (5.5 mmol/L) glucose. 24, 48, and 72 hours later radioimmunoassay was used to detect the insulin secretion index (ISI). 72 h later, the concentration of insulin in the cells was detected with radioimmunoassay. The contents of oxidative stress markers, nitrotyrosine (NT) and 8-hydroxy-2-deoxyguanosine (8-OHdG) were detected. Real-time PCR was used to detect the mRNA expression of peroxiredoxin 1 (PDX-1), ATF-4, one of the transcription factors of the family bZIP, and insulin. Western blotting was used to detect the protein expression of ATF-4. RESULTS: The ISI of the IHG and SHG groups decreased time-dependently, The ISI of IHG and SHG groups were 0.64 +/- 0.11 and 1.31 +/- 0. 04 respectively, both significantly lower than that of the control group (1.67 +/- 0.23, both P < 0.05). The intracellular insulin contents of the IHG and SHG groups were (10.91 +/- 0.14) and (11.08 +/- 0.03) +/- U/microg respectively, both significantly lower than that of the control group [(12.37 +/- 0.37) microU/microg, both P < 0.05]. The intracellular concentrations of 8-OHdG and NT of the SHG and IHG groups, were significantly higher than those of the control group (all P < 0.01), and those of the IHG group were significantly higher than those of the SHG group (both P < 0.05). The mRNA and protein expression levels of ATF-4 of the IHG group were all significantly higher than those of the control group (all P < 0.05) and those of the IHG group were significantly higher than those of the SHG group (both P < 0.05). CONCLUSION: IHG and SHG induce severe impairment in pancreatic islet beta cell functions, especially IHG, which is closely associated with the aggravation of oxidative stress and endoplasmic reticulum stress triggered by intermittent high glucose.

[Association of stroke and different combinations of metabolic syndrome components in Chinese adults].

OBJECTIVE: To analyze the association of stroke and metabolic syndrome as well as its component combinations in Chinese adults. METHODS: Logistic regression was used to analyze the data, including anthropometric measurement, fasting plasma glucose (FPG), blood lipids, and histories of smoking, drinking, and anamnesis, of 47,414 subjects, 22,305 males and 25,105 females, aged 20-75, obtained from Chinese National Health and Nutrition Survey in 2002. RESULTS: (1) Blood pressure and waist circumference were the most important factors associated with stroke. Along with the clustering of the risk factors, the subjects became more liable to suffer from stroke. Logistic regression showed that after adjustment for age, sex, smoking status, and LDL-C level, the odd ratio (OR) values of the individuals with one, two, three, and four or more factors were 3.01 (1.89-4.81) ,4.37 (2.72-7.01), 9.20 (5.75-14.73), and 13.09 (7.98-21.49) respectively. (2) The combinations of raised hypertension plus hyperglycemia and low LDL-C and central obesity were the most hazard groups, with the OR values of 16.58 (95% CI 8.78-31.32) for stroke. The OR value for the full metabolic syndrome was 10.79 (95% CI 6.81-17.10). Hypertriglyceridemia was not an independent risk factor of stroke. (3) The relationships of metabolic risk factors and stroke were various among different age groups. Stroke was not related with blood glucose, blood pressure, serum lipids, and obesity in the subjects under 35; in those aged 35-55, diastolic Bp and low HDL-C were most significantly related to stroke; as for those above 55, systolic Bp and waist circumference were most significantly related to stroke. CONCLUSION: Central obesity cored metabolic syndrome is an important risk factor of stroke. Different combinations of the components attribute variously to stroke. In people above middle age, stroke is related to metabolic risk factors.

[Do isolated hypertension and metabolic syndrome have equal risk of stroke in Chinese adults?].

OBJECTIVE: To analyze whether isolated hypertension and metabolic syndrome ( Based on the 2005 IDF criteria) have equal risk on stroke in Chinese adults. METHODS: 25194 subjects (25-75 years old) from Chinese National Health and Nutrition Survey in 2002 were divided into control group, isolated hypertension ( i-HTN) group, metabolic syndrome (MS) without hypertension ( non-HTN/MS) group , MS with hypertension (HTN/MS) group. The clinical features and risk for stroke ( using multiple logistic stepwise regression analysis) were compared among 4 groups. RESULTS: (1) The clinic features in the i-HTN group was non-central obesity, and its plasma glucose, triglyceride 9TG), high density lipoprotein cholesterol ( HDL-C) levels were normal . (2) The prevalence of stroke in control group , i-HTN group, non-HTN/MS group and HTN/MS group was 0.14%, 1.27%, 1.19% and 2.14%, respectively. (3) After adjustment for age, sex, smoking, low density lipoprotein cholesterol level, logistic regression analysis showed that the i-HTN group, non-HTN/MS group and HTN/MS group had higher risk of stroke compared with the controls, the odd ratio (OR) were 4.18, 8.00, 8.69 (P < 0.01), respectively. Compared with i-HTN group, OR in HTN/MS group was 2.05, while no difference was found between i-HTN group and non-HTN/MS group ( P>0.05). (4) Among different components of the MS, hypertension (OR 2.33), central obesity (OR 2.09), low HDL-C (OR 1.69), hyperglycemia (OR 1.66) except hypertriglyceridemia were all significantly related to stroke (P < 0.01). CONCLUSION: (1) MS and hypertension were an independent risk factor for the development of stroke in Chinese adults. (2) Though there was no clinical features of insulin resistance in i-HTN group, it was observed that the i-HTN and non-HTN/MS had equal contribution to stroke. The risk of stroke will be further increased if hypertension included in the MS.

Prevalence and risk factors of peripheral arterial disease in diabetic patients over 50 years old in China.

OBJECTIVE: To investigate the prevalence of peripheral arterial disease (PAD) in China type 2 diabetic patients and to demonstrate the relationships between putative risk factors and PAD. METHODS: In total 1,397 type 2 diabetic patients aged 50 years and older were enrolled and determined ankle-brachial index (ABI) and brachial-ankle pulse wave velocity (baPWV) in 15 Class III Grade A hospitals in 7 major cities of China. RESULTS: Mean patient age was 63.7 +/- 8.2 years and mean duration of diabetes mellitus was 9.39 +/- 7.4 years. Two hundreds and seventy-two (19.47%) patients were diagnosed as PAD by ABI < 0.9, 122 (18.37%) in male and 150 (20.46%) in female. PAD patients had a significantly longer duration of diabetes mellitus, higher hemoglobin A1c, and a significantly lower mean body mass index than non-PAD ones. Aging, smoking, and systolic blood pressure were found to be positively related with the prevalence of PAD. In terms of lipid profiles, no variable was found to relate with PAD. Notably, baPWV showed as the same significant guiding index for PAD, almost matched with ABI. CONCLUSIONS: PAD is a common complication in China type 2 diabetic patients. Therefore, PAD screening and treatment should be emphasized for diabetic patients with high risk factors.

[Analysis of peripheral arterial obstructive disease related factors among diabetic population aged > or = 50].

OBJECTIVE: To analyze the peripheral arterial obstructive disease (PAD) related factors among diabetic population aged > or = 50 in China. METHODS: The clinical data of 1397 diabetic patients aged > or = 50 with at least one of the following risk factors: smoking, hypertension, and hyperlipidemia, from 15 Class III Grade A hospitals in 7 major cities of China were collected. Diagnosis of PAD was based on the ankle brachial index (ABI) < 0.9, and diagnosis of arteriosclerosis was based on pulse wave velocity (PWV) > 1400 cm/s. Regression studies were made to analyze the relations among PAD and various risk factors: age, sex, body mass index (BMI), smoking, hypertension, hyperlipidemia, history of cerebral vascular disease (CVD), history of ischemia heart disease (IHD) etc. RESULTS: The current prevalence rate of PAD was 19.47% among the 1397 patients, 18.3% (122/664) among the male patients, and 20.4% (150/733) among the female patients. The prevalence of PAD in the patients aged > or = 70 was as high as 31.9%. The duration of diabetes course was positively correlated with the prevalence of PAD (chi2 = 11.9, P = 0.0026). The ABI abnormality rate was 15.78% among those with a diabetic course of 5 years and was 23.84% among those with a diabetic course of 10 years. The abnormal ABI rate of the patients with CVD was 30.57%, significantly higher than that of hose without CVD (17.29%, chi2 = 21.49, P < 0.0001). The abnormal ABI rate of the patients with IHD was 24.64%, significantly higher than that of the patients without IHD (18.20%, chi2 = 5.85, P = 0.0155). The HbA1c value of the PAD patients was significantly higher than that of the patients without PAD (chi2 = 5.10, P = 0.0239) Odd risk analysis showed that age increase of 10 years increased the PAD risk by 1.64 times (OR = 1.6444, P = 0.0001). The PAD risk of the smokers was 1.68 times higher than that of the non-smokers (OR = 1.6852, P = 0.0001). Increase of 10 mm Hg in systolic blood pressure (SBP) increased the PAD risk by 1.19 times (OR = 1.1926, P = 0.01). The PAD risk of the patients with abnormal HbAlc was 2.44 times higher than that of the patients with normal HbA1c (OR = 2.4473, P = 0.0001). One-year's increase of the hypertension course increased the PAD risk by 1.02 times (OR = 1.0194, P = 0.03). Logistic analysis indicated that the relations among PWV and the risk factors were almost the same among ABI abnormality and the risk factors. CONCLUSION: Approximately one fifth of diabetic patients aged > or = 50 in China suffer from PAD. Age, course of diabetes, blood glucose level, SBP, IHD, and CVD are risk factors for PAD. Early intervention and treatment of hypertension and hyperglycemia, and quitting smoking are important in reducing the occurrence of PAD. ABI and PWV are not only diagnostic means for PAD, but also alarm guide indexes for cerebral vascular disease (CVD).

[Compensated hyperinsulinemia based on selective insulin resistance predicts elevation of blood pressure in non-diabetic adults].

OBJECTIVES: To investigate if hyperinsulinemia or insulin resistance could predict the elevation of blood pressure in non-diabetic adults. METHODS: One hundred and seventy non-diabetic adults (NGT 107, IGT 63) were included based on the screen by OGTT in 1986. Height, weight, blood pressure were measured. Plasma glucose and insulin concentration at 0.60 and 120 min during OGTT were determined at baseline. All the subjects were followed for six years with blood pressure and plasma glucose examined at the end of the study. Subjects worsening to diabetes were excluded. Insulin area under-curve (INSAUC) and insulin sensitivity index [IAI = (1/FINS x FPG)] were calculated. Stepwise regression analysis was performed to evaluate the effects of INSAUC and insulin sensitivity to the elevation of blood pressure. RESULTS: Both SBP and DBP levels at the end of the study were increased with increased INSAUC baseline. The SBP were (119.5 +/- 2.3), (122.1 +/- 2.5), (129.4 +/- 2.4) and (128.3 +/- 2.6) mmHg, and the DBP were (78.6 +/- 1.6), (79.7 +/- 1.7), (85.2 +/- 1.4) and (84.0 +/- 1.0) mmHg from the lowest to the highest quartiles of INSAUC respectively. Pearson correlation analysis showed Age, SBP, DBP, BMI, FINS, INS1h, INSAUC at baseline were positively correlated to blood pressure levels at the end of the study. After the adjustment of Age, sex, BMI, smoking, PG2 h and blood pressure at baseline, the INSAUC was significantly correlated to blood pressure six years later, while the insulin sensitivity index was not. CONCLUSION: The compensated hyperinsulinemia based on selective insulin resistance rather than insulin resistance to glucose per se could predict the elevation of blood pressure in nondiabetic adults.