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Objective@#To examine associations of 25-hydroxyvitamin D [25(OH)D] concentrations with sex hormone levels and cardiovascular risk factors.@*Methods@#A total of 697 male subjects were obtained from the thyroid disorders, lodine status and diabetes: a national epidemiological survey-2014 (TIDE) research--Henan sub-center survey through multistage stratified cluster random sampling from December 2015 to March 2016. The associations between 25(OH)D and sex hormones or cardiovascular risk factors were analyzed by linear regression analyses.@*Results@#The age of the subjects was (46.6±15.9) years (19-85 years). Proportions of vitamin D deficient, vitamin D intermediate and vitamin D optimal were 9.3%, 13.1% and 77.6%, respectively. More subjects with vitamin D deficient were in urban area than in rural area (13.3% vs. 5.7%, P=0.001). After fully adjusting for age, residence area, economic status, education, body mass index, waist circumference, homeostasis model assessment of insulin resistance (HOMA-IR), hypertension, diabetes, triglyceride, high-density lipoproteincholesterol, total cholesterol, low-density lipoprotein cholesterol and uric acid, linear regression analyses showed that every 25 nmol/L increase in 25(OH)D levels increased lg FT(FT=free testosterone) by 0.013ng/L (β=0.013, P=0.036), lg DHT (DHT=dihydrotestosterone) by 0.030 ng/L (β=0.030, P=0.019), and lg AD (AD=androstenedione) by 0.019 μg/L (β=0.019, P=0.008). After fully adjusting for age, residence area, economic status and education, every 25 nmol/L increase in 25(OH)D levels lowered glycosylated hemoglobin A1c (HbA1c) by 0.051% (β=-0.051, P=0.027).@*Conclusions@#Higher 25(OH)D concentrations in men were associated with higher FT, DHT, AD and lower HbA1c levels.
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To examine associations of 25?hydroxyvitamin D [25(OH)D] concentrations with sex hormone levels and cardiovascular risk factors. Methods A total of 697 male subjects were obtained from the thyroid disorders, lodine status and diabetes: a national epidemiological survey?2014 (TIDE) research??Henan sub?center survey through multistage stratified cluster random sampling from December 2015 to March 2016. The associations between 25(OH)D and sex hormones or cardiovascular risk factors were analyzed by linear regression analyses. Results The age of the subjects was (46.6 ± 15.9) years (19?85 years). Proportions of vitamin D deficient, vitamin D intermediate and vitamin D optimal were 9.3%, 13.1% and 77.6%, respectively. More subjects with vitamin D deficient were in urban area than in rural area (13.3% vs. 5.7%, P=0.001). After fully adjusting for age, residence area, economic status, education, body mass index, waist circumference, homeostasis model assessment of insulin resistance (HOMA?IR), hypertension, diabetes, triglyceride, high?density lipoproteincholesterol, total cholesterol, low?density lipoprotein cholesterol and uric acid, linear regression analyses showed that every 25 nmol/L increase in 25(OH)D levels increased lg FT(FT=free testosterone) by 0.013ng/L (β=0.013, P=0.036), lg DHT (DHT=dihydrotestosterone) by 0.030 ng/L (β=0.030, P=0.019), and lg AD (AD=androstenedione) by 0.019 μg/L (β=0.019, P=0.008). After fully adjusting for age, residence area, economic status and education, every 25 nmol/L increase in 25(OH)D levels lowered glycosylated hemoglobin A1c (HbA1c) by 0.051% (β=-0.051, P=0.027). Conclusions Higher 25(OH)D concentrations in men were associated with higher FT, DHT, AD and lower HbA1c levels.
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<p><b>OBJECTIVE</b>To compare the predictive value of liver enzymes and alcohol consumption for determining risk of type 2 diabetes (T2DM).</p><p><b>METHODS</b>A cross-sectional study was conducted in Zhengzhou with a total of 2, 693 men.Participants' height, weight, and histories of smoking and drinking were recorded. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT) and blood glucose, as well as related metabolic indexes were detected.</p><p><b>RESULTS</b>Moderate daily alcohol consumption (more than 35 g ethanol/week and less than 140 g ethanol/week) decreased the risk of type 2 diabetes (OR =0.376, 95% CI:0.306 -0.463, P less than 0.05) but increased risk for higher levels of GGT and ALT (OR GGT =3.012, 95% CI:2.357-3.849, Pless than 0.01; ORALT =1.473, 95% CI:1.043-2.081, Pless than 0.05). In joint analyses of alcohol consumption and liver enzymes, the group of nondrinkers/light drinkers (less than or equal to 35 g ethanol/week) in the fourth quartile of GGT levels had the highest risk for type 2 diabetes (OR =12.219, 95% CI:6.217-24.016, P less than 0.01). The relationship of ALT and daily alcohol consumption with the risk of type 2 diabetes was almost the same as that of GGT (nondrinkers/light drinkers in the fourth quartile of ALT levels (OR =5.357, 95% CI:3.070-9.350, P less than 0.0 1).</p><p><b>CONCLUSION</b>GGT, ALT and daily alcohol consumption were independently associated with risk of type 2 diabetes. Nondrinkers/light drinkers with the highest levels ofGGT orALT were at high risk of type 2 diabetes.</p>
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Humans , Male , Alanine Transaminase , Alcohol Drinking , Aspartate Aminotransferases , Blood Glucose , Cross-Sectional Studies , Diabetes Mellitus, Type 2 , Liver , Risk Factors , Smoking , gamma-GlutamyltransferaseABSTRACT
Objective To study the effect and mechanism of forkhead transcriptionfactor O1( FoxO1) on proliferation of rat mesangial cells(MCs) cultured under high glucose conditions. Methods Constructing lentiviral vectors of LV-CA-FoxO1 and LV-siRNA-FoxO1 were used to upregulate or downregulate FoxO1. Moreover, negative control LV-NC-FoxO1 was also constructed. Rat MCs were separately cultured in normal glucose(5. 6 mmol/ L, NG group), only high glucose(30 mmol/ L, HG0 group), LV-NC-FoxO1 with HG(HG1 group),LV-CA-FoxO1 with HG (HG2 group), and LV-siRNA-FoxO1 with HG(HG3 group) for 72 h. MTT assay and flow cytometrywas were used to analyze cell proliferation and cell cycle distribution. The expression of FoxO1, cyclin-dependent kinase inhibitor (p27), cyclinD1, and cyclin-dependent kinase 4( CDK4) were detected by QRT-PCR and Western blot. Results The MCs proliferation rate in HG0 group was faster than that in NG group. Besides, there were no statistical differences in FoxO1 expression and proliferation rate of MCs between HG0 group and HG1 group. Nevertheless, LV-CA-FoxO1 promoted cell cycle arrest at the G1 phase and attenuated proliferation rate, along with upregulation of FoxO1 and p27 and downregulation of cyclin D1 and CDK4 in HG2 group ( all P < 0. 05). Moreover, degradation of FoxO1 by LV-siRNA-FoxO1 stimulated hyperproliferation of MCs, associating with decline of p27 and increase of cyclin D1 and CDK4 in HG3 group(all P<0. 05). Conclusion The proliferation of MCs induced by high glucose is regulated by utilizing transgenic technology targeted and regulated FoxO1 expression and consequently through FoxO1 / p27 signaling pathway. These findings indicate that FoxO1 seems to be a new therapeutic target for early diabetic nephropathy.
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Objective To clarify the clinical features and genetic background of a kindred of primary pigmented nodular adrenocortical disease (PPNAD).Methods Detailed clinical characteristics and laboratory test results from a ten-year old girl diagnosed as PPNAD were collected.Seven members of her family were screened for Cushing syndrome and Carney complex,and their blood DNA was extracted and sequenced for PRKAR1A,PDE11A,PDE8B and CTNNB1 mutations with ABI3730.Results The girl presented with symptoms and signs of hypercortisolism,while no features of Carney complex were observed.Hypercortisolemia,suppressed corticotrophin and high urinary free cortisol level were revealed.Cortisol level could not be suppressed both in high and low dose dexamethasone suppression test.The diagnosis of adrenocorticotrophic hormone (ACTH)-independent Cushing syndrome was established.Image and pathology of adrenal glands were in accordance with PPNAD.Other family members showed no evidence of Cushing syndrome or Carney complex.DNA sequencing showed that the patient harbored a missense mutation,C18G.Her father and younger sister were proved to be carriers of this mutation.Conclusion A Chinese PPNAD family was identified clinically and genetically,and a novel missense mutation of PRKAR1A was found.
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Objective To evaluate the association between serum 25-hydroxyvitamin D3 [25 (OH) D3],parathyroid hormone,and arterial stiffness in patients with type 2 diabetes.Methods Serum 25 (OH) D3 and parathyroid hormone(PTH) were determined in a cross-sectional sample of 258 patients aged 30 years and over.Arterial stiffness was assessed by pulse wave velocity(PWV) obtained with a VP-1000 pulse wave unit.Fasting plasma HbA1c,lipid profile,calcium,and high sensitive-C reactive protein were determined.Results (1)The prevalence of vitamin D3 deficiency was high(79.84％) in patients with type 2 diabetes.(2) Those with lowered serum vitamin D3 levels had raised PWV [(1610.76 ± 142.70 vs 1527.95 ± 58.02) cm/s,P＜0.05].(3) Multiple stepwise regression analysis showed that 25 (OH) D3 was an impact factor of PWV risk score,which was independent of age,duration of diabetes,and systolic blood pressure(β =-0.256,P＜0.01).(4) Serum PTH was positively correlated with PWV (r =0.210,P ＜ 0.05) and systolic blood pressure (r =0.229,P ＜ 0.05),but negatively correlated with 25 (OH) D3 (r =-0.153,P ＜ 0.05).Conclusions 25 (OH) D3 deficiency is common in patients with type 2diabetes,and a low serum 25 (OH) D3 level is significantly associated with increased arterial stiffness in these patients.The association of serum PTH with arterial stiffness may result via changes in vitamin D and blood pressure.
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Streptozotocin-induced diabetic rats were treated with resveratrol for 12 weeks.Compared with group of diabetic rats without treatment,the levels of urine albumin,serum creatinine,and blood urea nitrogen were significantly decreased and pathological changes in kidney were improved in treatment group ( P＜0.05 ).The mRNA expressions of FoxO1 and catalase were higher and FoxO1 phosphorylation level in diabetic rats treated with resveratrol was lower than that in diabetic rats without treatment (P＜0.05),suggesting that resveratrol may protect the kidneys of diabetic rats via regulating expression of FoxO1.
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The methylation status of GNAS1 gene in pseudohypoparathyroidism type Ib patients was detected by methylation-specific PGR technique. There was an abnormal methylation of 1A region in all seven PHPIb patients. Loss of exon 1A methylation (imprinting defect) seems to be the cause of PHPIb.