The Impact of Insulin Upon Atherosclerosis

Rw, Stout

doi:10.1055/s-2007-1000791

Cited by 26 publications

(11 citation statements)

References 24 publications

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“…Fasting insulin could be a sign of hyperinsulinaemia or insulin resistance and may contribute to cardiometabolic risk [21]. In contrast to others [15], heritability of BMI, HOMA-IR, eGFR and that of the metabolic syndrome was not assessed in our study because heritability of calculated values has no or limited biological relevance.…”

Section: Discussionmentioning

confidence: 92%

Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study

Jermendy

Horváth

Littvay³

et al. 2011

Cardiovasc Diabetol

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BackgroundBoth genetic and environmental factors play a role in the pathogenesis of type 2 diabetes and cardiovascular diseases. The magnitude of genetic and environmental influences may vary in different populations and can be investigated by twin studies.MethodsIn this cross-sectional study, 101 (63 monozygotic and 38 dizygotic) adult twin pairs (n = 202; mean age: 44.3 ± 15.8 years) were investigated. Past medical history was recorded and physical examination was performed. Fasting venous blood samples were taken for measuring laboratory parameters. For assessing heritability of 14 cardiovascular risk factors, the structural equation (A-C-E) model was used.ResultsThe following risk factors were highly (> 70.0%) or moderately (50.0 - 69.0%) heritable: weight (88.1%), waist circumference (71.0%), systolic blood pressure (57.1%), diastolic blood pressure (57.7%), serum creatinine (64.1%), fibrinogen (59.9%), and serum C-reactive protein (51.9%). On the other hand, shared and unique environmental influences had the highest proportion of total phenotypic variance in serum total cholesterol (46.8% and 53.2%), serum HDL-cholesterol (58.1% and 14.9%), triglycerides (0.0% and 55.9%), fasting blood glucose (57.1% and 42.9%), fasting insulin (45.4% and 54.5%), serum uric acid (46.0% and 31.3%), and serum homocysteine (71.8% and 28.2%, respectively).ConclusionSome cardiometabolic risk factors have strong heritability while others are substantially influenced by environmental factors. Understanding the special heritability characteristics of a particular risk factor can substantiate further investigations, especially in molecular genetics. Moreover, identifying genetic and environmental contribution to certain cardiometabolic risk factors can help in designing prevention and treatment strategies in the population investigated.

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Section: Discussionmentioning

confidence: 92%

Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study

Jermendy

Horváth

Littvay³

et al. 2011

Cardiovasc Diabetol

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“…Since higher triglyceride and lower HDL levels are related to insulin resistance 10 , impaired insulin action may also contribute to the effect of smoking on coronary artery disease (CAD). There are compelling reasons why insulin might be considered a major risk factor for CAD [11][12][13] . In fact, hyperinsulinaemia has been demonstrated to be a risk factor for subsequent CAD in recent studies 14,15 .…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoking is Independently Associated with Markers of Endothelial Dysfunction and Hyperinsulinaemia in Non-diabetic Individuals with Coronary Artery Disease

Winkelmann

Boehm

Nauck

et al. 2001

Current Medical Research and Opinion

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“…Although a number of factors such as hyperglycaemia, dyslipidaemia, a procoagulant state, hyperinsulinaemia, glycation of proteins, oxidation or glycation of lipoproteins, as well as enhanced smooth muscle cell proliferation and foam cell formation, have all been suggested as possible links between diabetes and atherosclerosis [1], the increased risk of coronary heart disease among diabetic patients still remains largely unexplained.Hyperinsulinaemia could be directly involved in atherogenesis [2], although this possibility is fiercely debated [3][4][5][6]. In patients with insulin-dependent diabetes (IDDM) exogenous hyperinsulinaemia exists due to intermittent injections of large amounts of insulin [1], and in patients with non-insulin dependent diabetes (NIDDM) endogenous hyperinsulinaemia Diabetologia (1997) 40: 512-520 Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits Summary To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 IU of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection.…”

mentioning

confidence: 99%

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

1997

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Coronary heart disease and thus atherosclerosis is the leading cause of death among patients suffering from diabetes mellitus; men and women with diabetes have a three to fivefold higher coronary heart disease mortality or incidence rate compared with non-diabetic subjects [1]. Although a number of factors such as hyperglycaemia, dyslipidaemia, a procoagulant state, hyperinsulinaemia, glycation of proteins, oxidation or glycation of lipoproteins, as well as enhanced smooth muscle cell proliferation and foam cell formation, have all been suggested as possible links between diabetes and atherosclerosis [1], the increased risk of coronary heart disease among diabetic patients still remains largely unexplained.Hyperinsulinaemia could be directly involved in atherogenesis [2], although this possibility is fiercely debated [3][4][5][6]. In patients with insulin-dependent diabetes (IDDM) exogenous hyperinsulinaemia exists due to intermittent injections of large amounts of insulin [1], and in patients with non-insulin dependent diabetes (NIDDM) endogenous hyperinsulinaemia Diabetologia (1997) 40: 512-520 Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits Summary To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 IU of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection. Compared to placebo rabbits, insulin-treated rabbits had higher levels of insulin antibodies in plasma, similar levels of intermediate density, low density and high density lipoprotein cholesterol and similar activities of hepatic and lipoprotein lipase in post-heparin plasma, but lower levels of plasma C-peptide, blood glucose, postprandial plasma triglycerides, plasma cholesterol and very low density lipoprotein cholesterol. On univariate analysis, with and without adjustment for differences in plasma cholesterol levels between the two groups, there were no significant differences in extent or severity of atherosclerosis between insulin and placebo rabbits. Furthermore, after combining the results from all the rabbits to examine plasma insulin levels and the other variables mentioned above as predictors of atherosclerosis severity, plasma insulin level was not a predictor, on univariate or multiple linear regression analysis; the first ranked independent predictors were postprandial intermediate density lipoprotein cholesterol in the arch, and postprandial plasma triglyceride in both the thoracic and abdominal aorta. These results suggest that exogenous hyperinsulinaemia does not promote atherogenesis in cholesterol-fed rabbits, but that postprandial levels of intermediate density lipoprotein cholesterol or plasma triglycerides may be involved in atherogenesis. [Diabetologia (1997)

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The Impact of Insulin Upon Atherosclerosis

Cited by 26 publications

References 24 publications

Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study

Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study

Cigarette Smoking is Independently Associated with Markers of Endothelial Dysfunction and Hyperinsulinaemia in Non-diabetic Individuals with Coronary Artery Disease

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

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