Lipid intolerance in smokers

Axelsen, Mette; Eliasson, Björn; Joheim, E; Lenner, Ragnhild Arvidsson; Taskinen, Marja‐Riitta; Smith, Ulf

doi:10.1111/j.1365-2796.1995.tb00869.x

Cited by 89 publications

(62 citation statements)

References 28 publications

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“…It has been reported that the daytime blood pressure and average 24 hour blood pressure are higher on smoking days than on nonsmoking days (4). After the same fat load was given to smoking and nonsmoking subjects with normal fasting TG levels, serum TG increased significantly, while HDL-C decreased significantly in the smoking subjects (6). Following a glucose load, the blood glucose level increased significantly after smoking in smoking subjects, and insulin and C-peptide levels also increased significantly, while the blood glucose level increased only Nonobese subjects: body mass index < 25, obese subjects: body mass index ≥ 25 NS: nonsmokers, S: smokers Mean ± SD **: p < 0.02, ***: p < 0.01 The waist circumference of each group of nonobese subjects was significantly smaller than that of each group of obese subjects (p < 0.01).…”

Section: Discussionmentioning

confidence: 96%

“…Although it has been reported that smoking influences body mass index (BMI) (2) and arteriosclerotic diseases (3), as well as blood pressure (4,5), lipid metabolism (5,6) and glucose metabolism (7,8), it has not been clarified whether there is a difference in the prevalence of hypertension or metabolic disorders between nonobese and obese persons based on the presence or absence of smoking.…”

Section: Introductionmentioning

confidence: 99%

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Obesity and Smoking: Relationship with Waist Circumference and Obesity-Related Disorders in Men Undergoing a Health Screening

Mizuno

Okamoto

Sawada

et al. 2005

JAT

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This study investigated whether smoking habits had a differential influence on waist circumference and obesity-related disorders in nonobese and obese men. We investigated 359 men with smoking habits confirmed by their spouses, including 172 nonobese men (BMI < 25) and 187 obese men (BMI ≥ ≥ ≥ ≥ ≥ 25). There were 113 nonobese smokers and 129 obese smokers. Obesity-related disorders were defined as hypertension, dyslipidemia, hyperglycemia, hyperuricemia, or treatment for one or more of these disorders. Nonobese subjects showed no differences of age, BMI, and waist circumference between smokers and nonsmokers, but smokers had a higher incidence of obesity-related disorders. Obese smokers were younger than obese nonsmokers and had a larger waist circumference, but a similar prevalence of obesityrelated disorders. The prevalence of obesity-related disorders was similar between obese nonsmokers and smokers, but the smokers were younger. In nonobese subjects, smoking may increase obesity-related disorders by a mechanism other than visceral fat accumulation. In obese subjects, however, smoking may promote visceral fat accumulation. Further investigations will be necessary to better elucidate the relationship between the promotion of visceral fat accumulation in obese subjects by smoking and obesity-related disorders. J Atheroscler Thromb, 2005; 12: 199-204.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Obesity and Smoking: Relationship with Waist Circumference and Obesity-Related Disorders in Men Undergoing a Health Screening

Mizuno

Okamoto

Sawada

et al. 2005

JAT

View full text Add to dashboard Cite

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“…A standardized meal test (energy content 900 kcal/3.75 MJ; 51 g of fat) was performed as described before, 15 and glucose, insulin and blood triglyceride levels were followed for 8 h every 2 h. Safety evaluations (reporting of adverse events, physical examination, retinal photography, blood pressure, electrocardiogram, and clinical routine laboratory tests) were performed at regular intervals during the study. Selfmonitored blood glucose measurements (SMBG) were carried out during the titration period in order to avoid hypoglycaemia.…”

Section: Other Measurementsmentioning

confidence: 99%

Weight loss and metabolic effects of topiramate in overweight and obese type 2 diabetic patients: randomized double-blind placebo-controlled trial

et al. 2007

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Objective: To examine the metabolic effects and body composition changes after topiramate treatment of obese type 2 diabetic patients (DM2) for 11 months. Design and subjects: Thirty-eight DM2 on diet or sulfonylurea treatment participated in this randomized double-blind placebocontrolled trial. Thirteen placebo-treated and nine topiramate-treated patients completed the trial. Patients were randomized to treatment with topiramate 96 mg b.i.d. or placebo (6-week run-in phase, 2-months titration phase, 9-months maintenance phase). Measurements: Insulin sensitivity was measured with euglycaemic hyperinsulinemic clamps. Weight, HbA1c, fasting glucose, blood lipids and safety variables were measured at regular intervals. Body composition was determined with computerized tomography. Meal tests were performed to evaluate postprandial glucose and insulin levels. Three-day diet recalls were carried out to evaluate energy ingestion. Results: The mean age was 58.677.1 years, body weight 98.1716.1 kg, BMI 33.074.5 kg/m 2 , and glycosylated hemoglobin (HbA1c) 7.370.9%. In topiramate-treated patients, there were significant reductions in HbA1c (1.170.9%), fasting plasma glucose, body weight (À6.673.3%), as well as body fat, lean body mass, postprandial glucose and free fatty acid levels but there were no significant changes in insulin sensitivity. The daily average energy intake decreased more in the topiramate group than in the placebo group. Paresthesia and central nervous system-related side effects were the main causes for the dropout rate. Conclusions: Topiramate treatment of overweight DM2 reduced body weight and body fat, and was associated with a marked improvement in glycaemic control whereas no significant improvement in insulin-stimulated glucose uptake was demonstrated. Further studies are required to clarify whether this effect might occur through changes in insulin sensitivity in the liver and/or pancreatic insulin secretion.

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“…Jenkins et al 16 showed only a 2% higher fasting TG level in smokers than in nonsmokers among 924 men aged 50 to 59 years, in contrast to a 12% higher fasting TG level in younger smokers. Postprandial TG level was evaluated in 2 small studies: (1) Axelson et al 17 showed 50% greater TG response in habitual smokers. (2) Mero et al 18 showed that smoking raised retinyl esters and apoB-48, but not apoB-100.…”

Section: February 2001mentioning

confidence: 99%

Metabolic and Lifestyle Determinants of Postprandial Lipemia Differ From Those of Fasting Triglycerides

Sharrett

Heiss

Chambless

et al. 2001

ATVB

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Abstract-Despite the reported association of lipoprotein responses to a fatty meal with atherosclerosis, little is known about the determinants of these responses. Plasma triglyceride, retinyl palmitate, and apolipoprotein B-48 responses to a standardized fatty meal containing a vitamin A marker were measured in 602 Atherosclerosis Risk in Communities (ARIC) study participants. To focus on postprandial responses specifically, which have been reported to be related to atherosclerosis independently of fasting triglycerides, analyses for determinants of postprandial responses were adjusted for fasting triglycerides. Major determinants of fasting triglycerides, namely, diabetes, obesity, other factors related to insulin resistance, and male sex, were not independently associated with postprandial responses. Fasting triglycerides were the strongest predictor of postprandial lipids, but independent of triglycerides, the predictors of postprandial responses were smoking, diet, creatinine, and alcohol. To investigate these associations, we studied participants of the largest published study of atherosclerosis and postprandial lipemia. 1 The Atherosclerosis Risk in Communities (ARIC) postprandial lipemia study demonstrated in 602 men and women that asymptomatic carotid atherosclerosis was positively associated with postprandial triglycerides (TGs) independently of coronary risk factors and fasting TGs. 1 Markers of intestinally derived postprandial lipoproteins were also studied, because small studies had previously reported coronary disease associated with the apoB-48/apoB-100 ratio 3 and a retinyl palmitate (RP) marker of these lipoproteins. 4 However, these markers were not associated with carotid atherosclerosis in the present study or a more recent study. 2 Despite a lack of association with intestinally derived lipoproteins, our finding that atherosclerosis was associated with postprandial TGs independently of fasting TGs suggested that lipoprotein characteristics specific to the postprandial state are atherogenic. The large size of the ARIC study is needed to detect the independent determinants of postprandial responses, inasmuch as postprandial responses are closely correlated with fasting TGs: rϭ0.64 for TGs and 0.49 for RP in the ARIC study.

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Lipid intolerance in smokers

Cited by 89 publications

References 28 publications

Obesity and Smoking: Relationship with Waist Circumference and Obesity-Related Disorders in Men Undergoing a Health Screening

Obesity and Smoking: Relationship with Waist Circumference and Obesity-Related Disorders in Men Undergoing a Health Screening

Weight loss and metabolic effects of topiramate in overweight and obese type 2 diabetic patients: randomized double-blind placebo-controlled trial

Metabolic and Lifestyle Determinants of Postprandial Lipemia Differ From Those of Fasting Triglycerides

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