Smoking, oxidative stress and inflammation: Impact on resting energy expenditure in diabetic nephropathy

Agarwal, Rajiv

doi:10.1186/1471-2369-6-13

Cited by 62 publications

(47 citation statements)

References 38 publications

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“…Similarly, no significant difference in the waist-to-hip ratio between the smokers and non-smokers also indicates a non increasing risk of metabolic syndrome for smokers. The results are corroborated by Agarwal 37 and others 33 who reported a non significant difference in the waist-to-hip ratio between the smokers and non smokers.…”

Section: Discussionsupporting

confidence: 81%

Association between Smoking and Anthropometric Characteristics, Biochemical Markers, and Dietary Intake of Pakistani Male Adult Population

Paracha¹,

Khan²,

Vriesekoop³

et al. 2015

Adv Food Technol Nutr Sci Open J

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Background/Objectives: A community-based study was conducted to compare the nutritional status between smokers and non-smokers in association with dietary, biochemical and socioeconomic characteristics. Methods: A convenient sampling method was used to enroll 100 smokers and 99 non-smokers aged between 46 and 78 years from the urban and semi-urban areas of district Peshawar, Pakistan. Weight, height, waist and hip circumferences of the subjects were taken while body composition was determined by employing a Bodystat Analyzer. A blood sample was taken from each subject for the determination of serum vitamin A and zinc levels. Subjects were interviewed for a 24-hr dietary recall and demographic and socio-economic characteristics. Student's t-test and bivariate analysis were conducted to compare the mean differences and examine the association between different variables of smoker and non-smoker groups. Results: The results revealed that there was no significant (p>0.05) difference between the mean age, weight, height and body mass index of smokers and non smokers. However, the mean body fat, waist and hip circumference of the smokers were significantly (p<0.05) lower than the non-smokers. Conversely, the mean serum vitamin A (32.30±15.99 µg/dl) of smokers was significantly (p<0.05) higher than non-smokers (26.50±20.44 µg/dl) but the mean serum zinc concentration of smokers (99.76±27.42 µg/dl) was significantly lower than the non-smokers (108.25±32.20 µg/dl). Conclusions: The study concludes that anthropometric (body mass index), biochemical (vitamin A and zinc status), dietary (energy intake) and socio-economic (income, profession) characteristics failed to establish an association with smoking as most of the indicators of smokers are comparable to non-smokers.

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Section: Discussionsupporting

confidence: 81%

Association between Smoking and Anthropometric Characteristics, Biochemical Markers, and Dietary Intake of Pakistani Male Adult Population

Paracha¹,

Khan²,

Vriesekoop³

et al. 2015

Adv Food Technol Nutr Sci Open J

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“…These results are in keeping with previ- ous data showing that CS exerts proinflammatory and oxidant effects in other organs, such as the kidney and the pancreas. [23][24][25][26][27] Here, we demonstrate that CS exacerbates liver damage in a genetic model of NAFLD. Our results suggest that CS could exert deleterious effects in the liver, acting as a cofactor favoring the progression of chronic liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

et al. 2010

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The prevalence of cigarette smoking (CS) is increased among obese subjects, who are susceptible to develop nonalcoholic fatty liver disease (NAFLD). We investigated the hepatic effects of CS in control and obese rats. Control and obese Zucker rats were divided into smokers and nonsmokers (n ‫؍‬ 12 per group). Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. The effects of CS were assessed by biochemical analysis, hepatic histological examination, immunohistochemistry, and gene expression analysis. Phosphorylation of AKT and extracellular signal-regulated kinase (ERK) and quantification of carbonylated proteins were assessed by western blotting. As expected, obese rats showed hypercholesterolemia, insulin resistance, and histological features of NAFLD. Smoking did not modify the lipidic or glucidic serum profiles. Smoking increased alanine aminotransferase serum levels and the degree of liver injury in obese rats, whereas it only induced minor changes in control rats. Importantly, CS increased the histological severity of NAFLD in obese rats. We also explored the potential mechanisms involved in the deleterious effects of CS. Smoking increased the degree of oxidative stress and hepatocellular apoptosis in obese rats, but not in controls. Similarly, smoking increased the hepatic expression of tissue inhibitor of metalloproteinase-1 and procollagen-alpha2(I) in obese rats, but not in controls. C igarette smoking (CS) is considered a worldwide major cause of preventable morbidity and mortality. 1 The main clinical consequences of prolonged exposure to CS are chronic respiratory diseases, increased incidence of a variety of cancers, and increased risk of atherothrombotic clinical events such as myocardial infarction. 2 Hepatologists have traditionally paid scant attention to the deleterious effects of CS. This reflects the fact that smoking per se does not appear to cause liver injury and therefore is not considered a causative agent for chronic liver diseases. 3 However, there is in-

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“…Insulin secreted by beta-cells of Langerhans in pancreas, is the key hormone in the regulation of blood and tissue glucose homeostasis. Among the cluster of risk cascade in diabetes are obesity (20)(21)(22), insulin resistance (23)(24)(25)(26)(27), beta-cell dysfunction (28)(29), formation of AGEs and RAGEs, autooxidation of glucose, activation of protein kinase C, polyol pathway, hexosamine pathway, numerous intracellular metabolic disturbances (30)(31)(32) smoking (33)(34)(35)(36)(37) and genetic disposition (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Many of these abnormalities are intricately interconnected.…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species, reactive nitrogen species and antioxidants in etiopathogenesis of diabetes mellitus type-2

Singh

Mahadi

Roy

et al. 2009

Indian J Clin Biochem

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Diabetes mellitus type-2 (DMT-2) is a hyperglycemic retinopathy and embryopathy) or a-vascular (cataract and glaucoma etc). It has been proposed that all these abnormal events are initiated or activated by a common mechanism of superoxide anion, which is accompanied with generation of a variety of reactive oxygen species (ROS), reactive nitrogen specie (RNS) and resultant heightened oxidative stress (OS). Provoked OS causes IR and altered gene expressions. Hyperglycemia induces OS through multiple routes : a)stimulated polyol pathway where in d 30% glucose can be diverted to sorbitol and fructose, b)increased transcription of genes for proinflammatory cytokines and plasminogen activator inhibitor-1 (PAI-1) c) activation of protein kinase-C (PKC) leading to several molecular changes d)increased synthesis of Advanced Glycation End Products (AGEs) e)changes in a receptor far AGEs and f) autooxidation of

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Smoking, oxidative stress and inflammation: Impact on resting energy expenditure in diabetic nephropathy

Cited by 62 publications

References 38 publications

Association between Smoking and Anthropometric Characteristics, Biochemical Markers, and Dietary Intake of Pakistani Male Adult Population

Association between Smoking and Anthropometric Characteristics, Biochemical Markers, and Dietary Intake of Pakistani Male Adult Population

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

Reactive oxygen species, reactive nitrogen species and antioxidants in etiopathogenesis of diabetes mellitus type-2

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