A comparative study of insulin resistance and lipid profile among smokers and non smokers

 

K Kadhiresan¹, P M Abraham Sam Rajan^2*, N Ananthi³, M Rengaramani⁴

 

¹Tutor, B. R. Ambedkar Medical, Bangalore -560045, Karnataka, INDIA.

²Associate Professor, ³Professor, ⁴Professor and HOD, Department of Biochemistry, Saveetha Medical College, Saveethanagar, Thandalam, Chennai-602105, Tamil Nadu, INDIA.

Email: salomi.jayasam@gmail.com

 

Abstract               Background: Cigarette smoking is one of the leading preventable cause of mortality and morbidity in both developed and developing countries. The present study was aimed to evaluate insulin resistance and serum lipid profile among smokers and non smokers. Methods: 96 samples were collected from male smokers and non smokers. Lipid profile, plasma glucose, serum insulin and insulin resistance by HOMA IR was calculated for all the samples collected. Results and Conclusion: There was an increase in the insulin resistance among the moderate and heavy male smokers when compared to the non smokers which was significant statistically and there was no statistical significant increase among the light smokers. There was also an increase in the total cholesterol, triglycerides, LDL, VLDL and decrease in HDL which were statistically significant among the light, moderate and heavy smokers when compared with non smokers. The current study has established the effect of smoking as a risk factor for coronary vascular disease.

Key Words: HOMA - IR, Nicotine, Paraoxynase 1, Hyperinsulinemia.

 

 

INTRODUCTION

Cigarette smoking is acknowledged as one of the leading causes of preventable morbidity and mortality. Cigarette smoking is said to be responsible for 17% - 30% of all death from cardiovascular illness.¹ According to a survey conducted by WHO it states that in India 35% of all men and 3% of women are smokers. ⁽²⁾Cigarette smoking is responsible for many disorders like lung cancer, hypertension COPD, myocardial infarction, stroke and peripheral vascular diseases. Previous literature has shown that there is a relationship between the number of cigarettes smoked, abnormal alterations in the levels of lipids and cardio vascular disorders.³ Insulin resistance generally refers to resistance to the metabolic effects of insulin, including the suppressive effects of insulin on endogenous glucose production, the stimulatory effects of insulin on peripheral glucose uptake, ( predominantly skeletal muscle) and glycogen synthesis, and the inhibitory effects of insulin on adipose tissue lipolysis.⁴ A recent study have showed that cigarette smoking favoured insulin resistance and dyslipidemia and an increased risk for coronary artery disease.⁵ The aim of the present study is to analyse fasting insulin levels, lipid profile, and calculation of insulin resistance by HOMA IR method among male smokers and non smokers and to evaluate the relationship between the number of cigarette smoked and the duration of smoking.

 

MATERIALS AND METHODS

The study was conducted with 96 male individuals in the department of biochemistry from those attending the out patient department for master health check up at Saveetha medical college and hospital, Thandalam, Chennai. Individuals with diabetes mellitus, hypertension, hypercholesterolemia, alcoholism and obesity were excluded from the study. After getting informed consent, 5ml of fasting blood samples were collected from all the participants. The blood samples were analysed for the estimation of parameters like fasting plasma glucose, total cholesterol, triglycerides, VLDL and HDL in Diasys fully automated analyser and LDL was calculated using Friedwalds equation. Serum fasting insulin was analysed by CLIA. HOMA - IR was (Homeostasis model assessment - Insulin resistant) was calculated by the formula⁶

The samples were divided into 2 groups as Group - I and Group - II⁷

Group I: Comprised of 24 male non smokers

Group II: Comprised of 72 male smokers which is divided into 3 sub groups depending on the number of cigarettes smoked per day⁷

Group II A: Light smokers (n = 24) - (smoking less than 10 cigarettes per day)

Group II B: Moderate smokers (n = 24) – (smoking 11 - 20 cigarettes per day)

Group II C: Heavy smokers (n = 24) - (smoking more than 20 cigarettes per day)

The samples were analyzed statistically using descriptive and interferential test using SPSS for windows (version 17) by ANOVA with TUKEY HSD method. The study was carried out over a period of 6 months after obtaining the approval from the Institutional Ethical Committee.

RESULTS

 

Table 1: Levels of fasting serum insulin and HOMA IR among non smokers and cigarette smokers

NS = Not significant

 

Table 2: Comparison levels of serum lipid profile among non smokers and cigarette smokers

DISCUSSION

In the current study it is evident from Table 1 that the degree of insulin sensitivity quantitated by HOMA IR was lower among moderate and heavy smokers when compared with non smokers which is statistically significant and there was no statistical significant difference in the HOMA IR among the light smokers and non smokers. Few studies conducted have shown that there was an increased insulin resistance and hyperinsulinemia in non diabetic chronic smokers when compared with non smokers.⁸ Some studies have demonstrated the features of Insulin Resistance Syndrome (IRS) and the extent of metabolic abnormalities were correlating with the severity of cigarette smoking.⁹ Cigarette smoking can induce insulin resistance¹⁰ and impaired glucose tolerance¹¹ among healthy smokers. The reasons for impaired insulin sensitivity among smokers may be due to increase in the levels of counter regulatory hormones and increased sympathetic nerve activity.¹² According to some studies the levels of catecholamines are raised among smokers which are potent insulin antagonistic hormones and also have long term effects on cellular synthesis of insulin regulated proteins, including the glucose transport proteins GLUT 4.¹³ Studies have shown that the nicotine present in cigarette smoke results in the expression of neuronal nicotinic acetylcholine receptors ( nAChRs) on many non neuronal cell types including pancreatic islet cells that impairs the sensitivity of insulin.¹⁴ Few studies have shown that,  when the concentration of nicotine exposure exceeds above 1µmol/L inhibits glucose induced insulin secretion in isolated human islets.¹⁵ Table 2 shows that there is a statistically significant increase in the levels of total cholesterol, triglycerides, VLDL, LDL and statistically significant decrease in the levels of HDL among smokers group II A, II B and II C when compared to non smokers group I. Our results were consistent with few studies which shows the association of abnormal lipid profile among smokers and was dependent on the number of cigarettes smoked.¹⁶ Smoking decreases the levels of oestrogen that leads to decreased HDL levels.¹⁷ Studies have demonstrated that cigarette smoking decreases the activity of lipoprotein lipase that leads to increased levels of LDL¹⁸ and also decreases the activity of lecithin cholesterol acyl transferase leading to decreased HDL.¹⁹ The polymorph enzyme, human serum paraoxanase 1 (PON1) has a role in decreasing the lipid peroxidation during LDL oxidation in the presence of HDL modification by lipid peroxidase.²⁰ Cigarette smoking inhibits the activity of PON1 and hence the antioxidant defence mechanism is compromised.²¹

 

CONCLUSION

The current study has established the effect of smoking as a risk factor for cardio vascular disease with decrease insulin sensitivity and increase in total cholesterol, triglycerides, LDL and VLDL and decrease in HDL.

 

ETHICAL APPROVAL

This prospective study was carried out at clinical biochemistry lab of Saveetha medical College and hospital, Chennai over a period of six months after obtaining the approval from the Institutional Ethical Committee. The article does not contain any studies with human participants or animals performed by any of the authors.

 

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