| 1. |
- Mero, N., et al.
(författare)
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Postprandial elevation of ApoB-48-containing triglyceride-rich particles and retinyl esters in normolipemic males who smoke
- 1997
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Ingår i: Arterioscler Thromb Vasc Biol. - 1079-5642. ; 17:10, s. 2096-102
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Tidskriftsartikel (refereegranskat)abstract
- Smokers have an increased risk for coronary artery disease (CAD), which can only partly be explained by fasting lipoprotein changes. Recent studies have indicated that smokers express metabolic abnormalities characteristic of insulin resistance syndrome. A preliminary study reported an increased postprandial triglyceride (TG) response in smokers compared with nonsmokers. To investigate the effect of smoking on postprandial lipemia, a fat-rich mixed meal (837 kcal, 63 g of fat) was served to 12 healthy smokers and 12 controls with similar fasting lipoprotein profiles, body composition, and lifestyles. Blood was drawn before and 3, 4, 6, and 8 hours postprandially, and triglyceride-rich lipoprotein (TRL) fractions (chylomicrons, VLDL1, VLDL2, and IDL) were separated with density gradient ultracentrifugation. Pre- and postprandial TG, retinyl esters (RE), apolipoprotein B-48 (apoB-48) and B-100 (apoB-100) were measured in each fraction. Smokers showed a significantly increased postprandial TG response in chylomicrons, VLDL1, and VLDL2. The areas under the incremental curve (AUIC) of apoB-48 in chylomicrons (2.83 +/- 0.84 versus 0.56 +/- 0.17; P < .05) and VLDL1 (10.17 +/- 1.96 versus 2.95 +/- 2.44; P = < .01) were markedly higher in smokers than in controls. Changes of RE responses of all TRL fractions were consistent with those of apoB-48. Postprandial apoB-100 concentrations and lipolytic enzymes were similar between the two groups. In conclusion, smokers have the syndrome of impaired TG tolerance because of defective clearance of chylomicrons and their remnants. Prolonged residence time of atherogenic remnant particles may constitute a significant risk factor for CAD in smokers.
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| 2. |
- Axelsen, Mette, 1965, et al.
(författare)
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Lipid intolerance in smokers
- 1995
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Ingår i: J Intern Med. - 0954-6820. ; 237:5, s. 449-55
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES. Smokers have recently been shown to be insulin resistant and to exhibit several characteristics of the insulin resistance syndrome (IRS). In this study, we assessed fasting and postprandial lipid levels in healthy, normolipidaemic, chronic smokers and a matched group of non-smoking individuals. DESIGN. A standardized mixed meal (containing 3.78 MJ and 51 g of fat) was given in the morning after an overnight fast. The smokers were either abstinent from tobacco for 48 h or were allowed to smoke freely, including being allowed to smoke six cigarettes during the study. SUBJECTS. Twenty-two middle-aged, healthy male subjects, nine habitual smokers and 13 non-smoking control subjects, were recruited to the study. The smokers had all been smoking at least 10 cigarettes per day for at least 10 years. RESULTS. The smokers exhibited a lipid intolerance in that their postprandial increase in triglyceride levels was more than 50% higher than in the non-smokers' group. This lipid intolerance could not be discerned in the postabsorptive state because the fasting triglyceride levels were the same in both groups, while the smokers had significantly lower high-density lipoprotein (HDL) cholesterol. The peak postprandial triglyceride level correlated closely and negatively with fasting HDL cholesterol, indicating an impaired lipolytic removal capacity in smokers. CONCLUSIONS. Healthy, normotriglyceridaemic smokers exhibit an abnormal postprandial lipid metabolism consistent with lipid intolerance. It is suggested that postprandial hyperlipidaemia is a characteristic trait of the insulin resistance syndrome and that the defect in lipid removal is related to the low HDL cholesterol in this syndrome. The insulin resistance syndrome is likely to be an important reason for the increased propensity for cardiovascular disease in smokers.
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| 3. |
- Axelsen, Mette, 1965, et al.
(författare)
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Postprandial hypertriglyceridemia and insulin resistance in normoglycemic first-degree relatives of patients with type 2 diabetes.
- 1999
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Ingår i: Annals of internal medicine. - 0003-4819 .- 1539-3704. ; 131:1, s. 27-31
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Impaired ability to eliminate lipids in the postprandial state is an atherogenic trait associated with insulin resistance. OBJECTIVE: To assess insulin sensitivity and postprandial triglyceride metabolism in prediabetic persons. DESIGN: Cross-sectional study. SETTING: Sahlgrenska University Hospital, Göteborg, Sweden. PARTICIPANTS: 13 healthy, normotriglyceridemic men with two first-degree relatives with type 2 diabetes and 13 carefully matched controls without known diabetes heredity. MEASUREMENTS: Oral glucose tolerance test, insulin sensitivity (euglycemic clamp technique), and fasting and postprandial triglyceride levels after a mixed meal. RESULTS: Relatives of persons with type 2 diabetes were insulin resistant but had normal glucose tolerance. They exhibited postprandial hypertriglyceridemia; the 6-hour triglyceride incremental area under the curve was 50% higher than that of the control group (P = 0.037). CONCLUSIONS: These healthy male first-degree relatives of patients with type 2 diabetes are insulin resistant and exhibit postprandial lipid intolerance despite having normal fasting triglyceride levels. These characteristics, which occur in the absence of glucose intolerance, are associated with an increased risk for macroangiopathy.
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| 4. |
- Eliasson, Björn, 1959, et al.
(författare)
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Long-term use of nicotine gum is associated with hyperinsulinemia and insulin resistance
- 1996
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Ingår i: Circulation. - 0009-7322. ; 94:5, s. 878-81
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Insulin sensitivity and cardiovascular risk profile were examined in 20 healthy, nonobese, middle-aged men who were long-term users of nicotine-containing chewing gum and in 20 matched control subjects who did not use nicotine. METHODS AND RESULTS: Long-term use of nicotine-containing chewing gum was associated with insulin resistance and hyperinsulinemia. The degree of insulin sensitivity correlated negatively to the extent of nicotine use measured as plasma cotinine levels. CONCLUSIONS: These findings suggest that nicotine is the major constituent in cigarette smoke that leads to insulin resistance, metabolic abnormalities associated with the insulin resistance syndrome, and increased cardiovascular morbidity. Thus, the use of nicotine replacement therapy during smoking cessation should be transient and limited.
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| 5. |
- Eliasson, Björn, 1959, et al.
(författare)
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Smoking cessation improves insulin sensitivity in healthy middle-aged men
- 1997
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Ingår i: Eur J Clin Invest. - 0014-2972. ; 27:5, s. 450-6
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Tidskriftsartikel (refereegranskat)abstract
- Cigarette smokers have recently been shown to exhibit insulin resistance, dyslipidaemia and markers of the insulin resistance syndrome (IRS). The aim of this study was to examine the effects of smoking cessation on insulin sensitivity and IRS. Forty male, non-obese healthy smokers participated in this open parallel study with 8 weeks of follow-up. Seventeen subjects were able to stop smoking, while 23 subjects continued to smoke and served as a controls group. Anthropometric and metabolic data were measured. Degree of insulin sensitivity was determined with the euglycaemic hyperinsulinaemic clamp technique. Smoking cessation increased insulin sensitivity and improved the lipoprotein profile in spite of a modest increase in body weight. Initial smoking habits correlated positively with the increase in BMI as well as the improvements in the metabolic variables after smoking cessation. These data support the view that smoking causes insulin resistance and IRS, and also demonstrate that the beneficial metabolic effects of smoking cessation override the effects of an accompanying modest increase in body weight.
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| 6. |
- Eliasson, Björn, 1959, et al.
(författare)
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The insulin resistance syndrome and postprandial lipid intolerance in smokers
- 1997
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Ingår i: Atherosclerosis. - 0021-9150. ; 129:1, s. 79-88
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The effects of cigarette smoking on insulin resistance, postprandial lipemia following a mixed meal, lipoproteins and other aspects of the insulin resistance syndrome (IRS) were investigated in healthy middle-aged men. METHODS: 36 smoking and 25 age- and body mass index (BMI)-matched non-smoking men participated. They were non-obese (BMI < 27), healthy and without any medication. The smokers had been smoking more than 10 cigarettes per day for more than 20 years; the non-smokers had never been habitual smokers. Body composition and several metabolic and cardiovascular risk factors were studied, including the prevalence of small dense LDL-particles, lipoprotein and hepatic lipase activity and triglyceride levels after a mixed test meal. For determination of degree of insulin sensitivity the euglycemic hyperinsulinemic clamp technique was used. RESULTS: The smokers had lower HDL-cholesterol and lipoprotein A-I levels but higher fasting triglycerides, as well as an increased proportion of small dense LDL-particles and higher postheparin hepatic lipase activity. They also had higher levels of fibrinogen, plasminogen activator inhibitor 1 (PAI-1) activity and fasting and steady-state C-peptide levels during the clamp. The smokers were insulin resistant and lipid intolerant with an impaired triglyceride clearance after a mixed test meal. This lipid intolerance was not mirrored by fasting hypertriglyceridemia. CONCLUSIONS: This study, using the euglycemic hyperinsulinemic clamp technique, shows that smokers are both insulin resistant and lipid intolerant. The postprandial lipid intolerance is also seen in individuals with normal fasting triglyceride levels and is related to an increased prevalence of atherogenic small dense LDL. IRS is likely to be an important reason for the increased cardiovascular morbidity in smokers.
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| 7. |
- Svensson, Johan, 1964, et al.
(författare)
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Treatment of obese subjects with the oral growth hormone secretagogue MK-677 affects serum concentrations of several lipoproteins, but not lipoprotein(a).
- 1999
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 84:6, s. 2028-33
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Tidskriftsartikel (refereegranskat)abstract
- Obesity is associated with blunted GH secretion and an unfavorable lipoprotein pattern. The objective of this study was to investigate the effects of treatment with the oral GH secretagogue MK-677 on lipoproteins in otherwise healthy obese males. The study was randomized, double blind, and parallel. Twenty-four obese males, aged 18-50 yr, with body mass index greater than 30 kg/m2 and waist/hip ratio above 0.95 were treated with 25 mg MK-677 (n = 12) or placebo (n = 12) daily for 8 weeks. MK-677 treatment did not significantly change serum lipoprotein(a) [Lp(a)] levels. Serum apolipoprotein A-I and E (apoA-I and apoE) were increased at 2 weeks (P < 0.001 and P < 0.01 vs. placebo, respectively), but were not changed at study end. Serum total cholesterol and low density lipoprotein (LDL) cholesterol (LDL-C) levels were not significantly changed by MK-677 treatment. Serum high density lipoprotein (HDL) cholesterol (HDL-C) was increased at 2 weeks of MK-677 treatment (P < 0.01 vs. placebo), but not at 8 weeks. The LDL-C/HDL-C ratio was reduced after 8 weeks of MK-677 treatment (P < 0.05 vs. placebo). Mean LDL particle diameter was decreased at 2 weeks (P < 0.05 vs. placebo), but was unchanged compared with baseline values at 8 weeks (P = NS vs. placebo). The level of serum triglycerides was increased at 2 (P < 0.05 vs. placebo), but not at 8, weeks. Lipoprotein lipase activity in abdominal and gluteal sc adipose tissue was not affected by active treatment. In conclusion, treatment with the oral GH secretagogue MK-677 affected circulating lipoproteins. The effects on serum apoA-1, apoE, triglycerides, and mean LDL particle diameter were transient. At study end, the LDL-C/HDL-C ratio was decreased. MK-677 treatment did not significantly affect serum Lp(a) concentrations at the present dose and administration protocol.
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