Insulin Resistance In Smokers Research Articles

Early Detection of Insulin Resistance and Assorted Metabolic Dysfunctions through MicroRNA-141

Background: MicroRNAs (miRNAs) are non-coding RNAs. Previously we worked to investigate level of miRNA-141 in experimental animal model that were exposed with graded doses of nicotine as well we also found genetic variation among PPAR-γ , FTO, and ABCC8 genes with 25%, 24%, and 20% genetic variations in cardiometabolic smokers. Objective: present study was aimed to investigate level of miRNA-141 in human subjects designated as diabetic smokers and non-diabetic smokers. We further intended to explore conceivable interplay of miRNA-141 expression alteration with adipokine homeostasis and incidence of insulin resistance in participants. Methods: Serum was used to measure cotinine level and levels of leptin, adipokines, IL-6, MDA, HbA1c, insulin, G6PDH, hexokinase, and lipid profile. miRNA-141 expression level was determined in plasma. It was found that higher level of cotinine, higher glucose level were observed. Results: Interestingly this was found to be related with insulin resistance in smokers along with significantly increased HbA1c, leptin, IL-6, MDA and lipids levels, while, adiponectin, G6PDH, hexokinase and HDL levels were significantly lowered.

Effect of Withania somnifera on oxidative stress and insulin resistance in smokers

Effect of Withania somnifera on oxidative stress and insulin resistance in smokers

Nicotine and Insulin Resistance: When the Smoke Clears

Although cigarette smoking is associated with insulin resistance and an increased risk for type 2 diabetes (1), few studies have examined the metabolic and molecular effects of smoking cessation in humans. Epidemiological data from the Atherosclerosis Risk in Communities study in middle-aged men and women offer several insights into the relationship between smoking cessation and diabetes. This study suggests that individuals who quit smoking are at increased risk of type 2 diabetes and that this risk is highest in the first 2 years after smoking cessation, but that risk declines after this point until no excess risk is observed at 12 years after cessation. The increased risk of type 2 diabetes associated with smoking cessation seems to be partially mediated by weight gain (2,3). In this issue of Diabetes , Bergman et al. (4) examined the metabolic and molecular effects of smoking cessation (for 1–2 weeks) in young, lean, otherwise healthy college students, a population that is increasingly vulnerable to the effects of both cigarette smoking and second-hand smoke exposure. Their results suggest that skeletal muscle insulin resistance in smokers is associated with increased mammalian target of rapamycin (mTOR)/p70S6 K activity and insulin receptor substrate-1 (IRS-1) Ser636 phosphorylation by nicotine, and these effects are reversible with smoking cessation. Cigarette smoking increases energy expenditure (Fig. 1), and this effect may be mediated in part by the sympathetic nervous system (5). In addition, smoking enhances lipid mobilization. Hellerstein et al. (6) demonstrated that cigarette smoking acutely increased free fatty acid (FFA) and glycerol fluxes as well as circulating FFA concentrations due to …

Putative roles of circulating resistin in patients with asthma, COPD and cigarette smokers.

Aims: To investigate the hypothesis that circulating resistin reflects the degree of pulmonary inflammation, this study explores putative roles of resistin in patients with acute and stable inflammatory obstructive airway diseases and cigarette smokers. Methods: We determined complements C3, C4, fasting resistin, insulin, glucose and lipid profile; calculated insulin resistance (homeostasis model assessment (HOMA-IR) in patients with acute asthma exacerbation (n = 34); stable asthma (n = 26) and stable chronic obstructive pulmonary disease (COPD; n = 26), cigarette smokers (n = 81), and healthy control subjects (n = 42). We determined the associations between these variables and pulmonary function tests.Results: Patients with COPD, acute and stable asthma had significantly higher resistin and insulin than control subjects. Resistin, insulin, HOMA-IR, FEV1% and FEV1/FVC were significantly (p < 0.05) different between patients with acute asthma compared with stable asthma and COPD; smokers had similar levels of resistin, C3 and C4 as patients with asthma and COPD. In smokers, patientswith asthma or COPD, resistin showed significant inverse correlations with FEV1%; FEV1/FVC% and positive significant correlations with BMI and HOMA-IR. Logistic regression showed that resistin is associated (p < 0.05) with inflammatory obstructive airways disease − odds ratio (OR) = 1.22 and smoking OR = 1.18.Conclusion: Resistin may be a disease activity marker and may contribute to insulin resistance in smokers, asthma and COPD.

Putative Roles of Circulating Resistin in Patients with Asthma, COPD and Cigarette Smokers

Aims:To investigate the hypothesis that circulating resistin reflects the degree of pulmonary inflammation, this study explores putative roles of resistin in patients with acute and stable inflammatory obstructive airway diseases and cigarette smokers.Methods:We determined complements C3, C4, fasting resistin, insulin, glucose and lipid profile; calculated insulin resistance (homeostasis model assessment (HOMA-IR) in patients with acute asthma exacerbation (n= 34); stable asthma (n= 26) and stable chronic obstructive pulmonary disease (COPD;n= 26), cigarette smokers (n= 81), and healthy control subjects (n= 42). We determined the associations between these variables and pulmonary function tests.Results: Patients with COPD, acute and stable asthma had significantly higher resistin and insulin than control subjects. Resistin, insulin, HOMA-IR, FEV1% and FEV1/FVC were significantly (p&lt; 0.05) different between patients with acute asthma compared with stable asthma and COPD; smokers had similar levels of resistin, C3 and C4 as patients with asthma and COPD. In smokers, patientswith asthma or COPD, resistin showed significant inverse correlations with FEV1%; FEV1/FVC% and positive significant correlations with BMI and HOMA-IR. Logistic regression showed that resistin is associated (p&lt; 0.05) with inflammatory obstructive airways disease − odds ratio (OR) = 1.22 and smoking OR = 1.18.Conclusion: Resistin may be a disease activity marker and may contribute to insulin resistance in smokers, asthma and COPD.

High-Sensitivity CRP Reflects Insulin Resistance in Smokers

The elevation of high-sensitivity C-reactive protein (hs-CRP) is a strong risk factor for cardio-vascular disease (CVD) and is associated with insulin resistance. The hs-CRP concentration also increases in smokers known to be at a high risk for CVD. We examined whether hs-CRP concentra-tion reflects insulin resistance in smokers. The hs-CRP levels were measured in 121 male subjects (54 nonsmokers and 67 smokers) with a normal glucose tolerance. The hs-CRP concentration was compared to the homeostasis model assessment of insulin resistance (HOMA-IR) and other clinical variables related to insulin resistance. Smokers had a 64.5% higher hs-CRP concentration than nonsmokers (p<0.0001). In both nonsmokers and smokers, hs-CRP positively correlated with HOMA-IR (r=0.301, p<0.05 and r=0.312, p<0.01) and fasting insulin (r=0.281, p<0.05 and r=0.356, p<0.01). The correlation between hs-CRP and HOMA-IR or fasting insulin was stronger in smokers than in nonsmokers. In smokers, hs-CRP significantly correlated with BMI and HDL-cholesterol (r=0.386, p<0.01 and r=-0.307, p<0.05). Stepwise regression analysis revealed that BMI and HOMA-IR were significant predictors of hs-CRP in smokers (r=0.423, p<0.01). The hs-CRP concentration reflects insulin resistance in smokers. It would be preferable to consider insulin resistance in evaluating hs-CRP concentrations, even in smokers.

Cigarette smoking induces insulin resistance: Partly via ASP–C5L2 pathway?

Smoking is one of the main risk factors for cardiovascular disease. The smokers exhibit different degrees of insulin resistance. The pathway of acylation-stimulating protein (ASP) and its specific receptor, C5a-like receptor 2 (C5L2), involves in the effective clearance of plasma glucose and triglyceride. ASP and insulin play similar but distinct roles in adipose metabolism. High level of ASP is indicative of ASP resistance and insulin resistance. Low level of ASP indicates increased insulin sensitivity. We proposed that the abnormality of ASP–C5L2 pathway contributes to insulin resistance in smokers.

We-P11:72 High-sensitivity C-reactive protein and serum amyloid a reflect insulin resistance in smokers

We-P11:72 High-sensitivity C-reactive protein and serum amyloid a reflect insulin resistance in smokers

Decreased blood flow but unaltered insulin sensitivity of glucose uptake in skeletal muscle of chronic smokers

Chronic cigarette smoking is associated with dysfunction of the vascular endothelium. Smokers have also been shown to be insulin-resistant, at least in some studies. Since insulin-induced vasodilation is dependent on endothelial cell nitric oxide (NO) synthesis, we tested the hypothesis that decreased skeletal muscle blood flow causes insulin resistance in smokers. We studied 37 young normotensive normolipidemic nondiabetic men, of which 14 were smokers and 23 lifelong nonsmokers. The groups were similar with respect to age, body mass index (BMI), and maximal oxygen uptake (VO2max). Basal and insulin-stimulated femoral muscle blood flow was measured using [(15)O]H2O and insulin-stimulated muscle glucose uptake using [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET). Whole-body glucose uptake was measured using the hyperinsulinemic (insulin infusion 5 mU/kg x min)-euglycemic clamp technique. In the basal state, muscle blood flow was 51% lower in smokers (17 +/- 3 mL/kg muscle x min) versus nonsmokers (35 +/- 17 mL/kg x min, P < .0001). Insulin increased muscle blood flow comparably in both groups; the mean rate of insulin-stimulated blood flow was 30 +/- 10 and 55 +/- 38 mL/kg x min (P = .049), respectively. Whole-body and skeletal muscle glucose uptake were similar in both groups during insulin infusion. We conclude that muscle blood flow is lower in chronic smokers compared with nonsmokers under both fasting and hyperinsulinemic conditions. The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects.

Abstracts of Literature

Abstracts of Literature

Cardiovascular risk factors in relation to cigarette smoking: a population-based survey among Asians in Singapore

To investigate how cigarette smoking increases the risk of cardiovascular disease, risk factors were compared between 166 cigarette smokers and 312 non-smokers, in a random sample of males (Chinese, Malays and Asian Indians) aged 30–69 years from the general population of Singapore. There was adjusted for age and ethnic group. The prevalence of hypertension was lower in cigarette smokers (15.2%) than non-smokers (21.9%), with the difference reduced by adjustment for body mass index (BMI). Smokers had: lower mean serum HDL-cholesterol (0.76 versus 0.81 mmol/l) and higher mean serum fasting triglyceride (1.92 versus 1.71 mmol/l), which will increase atherosclerosis; higher mean plasma fibrinogen (2.75 versus 2.67 g/l) and plasminogen activator inhibitor 1 [PAI-1] (24.9 versus 22.2 ng/ml), which will increase thrombosis; and lower mean plasma vitamin C (4.4 versus 6.4 mg/l) and serum selenium (118 versus 123 μg/l), which may increase atherosclerosis. Adjustment for BMI slightly increased the differences for HDL-cholesterol, fasting triglyceride, fibrinogen and PAI-1, indicating that less generalised obesity among smokers reduces their increased cardiovascular disease risk. Smoking was not found to be related to: diabetes mellitus; serum total cholesterol, LDL-cholesterol, apolipoproteins A1 and B and lipoprotein(a); plasma factor VIIc and prothrombin fragment 1+2; and plasma vitamins A and E and serum ferritin. There was no evidence of increased insulin resistance in smokers, as measured by mean fasting serum insulin.

Insulin resistance in smokers is a function of smoking habits

Insulin resistance in smokers is a function of smoking habits