Insulin resistance is a cardiovascular risk factor in humans

Adeva‐Andany, María M.; Martínez-Rodríguez, Julia; González-Lucán, Manuel; Fernández‐Fernández, Carlos; Castro-Quintela, Elvira

doi:10.1016/j.dsx.2019.02.023

Cited by 185 publications

(160 citation statements)

References 89 publications

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“…The multivariate regression analysis found that age and WHR were risk factors for high-risk polyps in the colon. Studies have confirmed that WHR and HOMA-IR play important roles in the development of cardiovascular disease in diabetic and non-diabetic patients [20,21]. And the above results of this study Fig.…”

Section: Discussionsupporting

confidence: 85%

Plasma adiponectin, visfatin, leptin, and resistin levels and the onset of colonic polyps in patients with prediabetes

et al. 2020

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Background: Prediabetes is associated with a high risk of colon cancer, and abdominal obesity, which can result in the secretion of several obesity-related adipocytokines, is an independent influencing factor for colonic polyps in prediabetes subjects. However, the correlation between adipocytokine levels and colonic polyps in prediabetes subjects is unclear. This research explores the relationship between plasma adiponectin, visfatin, leptin, and resistin levels and the development of colonic polyps in prediabetes subjects. Methods: A total of 468 prediabetes subjects who underwent electronic colonoscopy examinations were enrolled in this study; there were 248 cases of colonic polyps and 220 cases without colonic mucosal lesions. Then, colonic polyps patients with prediabetes were subdivided into a single-polyp group, multiple-polyps group, low-risk polyps group, or high-risk polyps group. In addition, 108 subjects with normal glucose tolerance who were frequency matched with prediabetes subjects by sex and age were selected as the control group; 46 control subjects had polyps, and 62 control subjects were polyp-free. Plasma adiponectin, visfatin, leptin, and resistin levels were measured in all the subjects, and the related risk factors of colonic polyps in prediabetes subjects were analysed. Results: Plasma adiponectin levels were significantly lower in the polyps group than in the polyp-free group [normal glucose tolerance (9.8 ± 4.8 vs 13.3 ± 3.9) mg/L, P = 0.013; prediabetes (5.6 ± 3.7 vs 9.2 ± 4.4) mg/L, P = 0.007]. In prediabetes subjects, plasma adiponectin levels were decreased significantly in the multiple polyps group [(4.3 ± 2.6 vs 6.7 ± 3.9) mg/L, P = 0.031] and the high-risk polyps group [(3.7 ± 2.9 vs 7.4 ± 3.5) mg/L, P < 0.001] compared to their control groups. Plasma visfatin levels were higher in the polyps group and the multiple-polyps group than those in their control groups (P = 0.041 and 0.042, respectively), and no significant difference in plasma leptin and resistin levels was observed between these three pairs of groups (all P > 0.05). The multivariate logistic regression analysis showed that lower levels of plasma adiponectin was a risk factor for colonic polyps, multiple colonic polyps, and high-risk colonic polyps in prediabetes subjects.

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Section: Discussionsupporting

confidence: 85%

Plasma adiponectin, visfatin, leptin, and resistin levels and the onset of colonic polyps in patients with prediabetes

et al. 2020

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“…Hyperinsulinemia and insulin resistance enhance the risk of cardiovascular disease, by inducing endothelial dysfunction, suppression of endothelial nitric oxide synthase (eNOS), and activation and promotion of calcium ion influx into smooth muscle cells, resulting in increased vascular tone, enhanced reabsorption of sodium ions in renal tubules, adhesion of macrophages to the vessel wall, and development of arterial lesions with increased lipoprotein lipase activity and cardiovascular disease marker of increased risk of cardiovascular disease in the general population and in patients with diabetes [95]. Although observational studies suggested an approximately linear relation between the severity of hyperglycemia and vascular damage, several large randomized controlled trials have shown that intense glycemic control per se does not decrease the risk of macrovascular/cardiovascular events [96]; indeed, insulin therapy may even increase the risk [95,97,98]. However, these trials were not randomized for insulin treatment, and treatment of CVD risk factors was not kept similar between patient subgroups.…”

Section: Detrimental Combination Of Hyperinsulinemia With Insulin Resmentioning

confidence: 99%

Insulin: too much of a good thing is bad

Kolb

Kempf

Röhling

et al. 2020

BMC Med

141

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Background: Insulin shares a limited physiological concentration range with other endocrine hormones. Not only too low, but also too high systemic insulin levels are detrimental for body functions. Main body: The physiological function and clinical relevance of insulin are usually seen in association with its role in maintaining glucose homeostasis. However, insulin is an anabolic hormone which stimulates a large number of cellular responses. Not only too low, but also excess insulin concentrations are detrimental to the physiological balance. Although the glucoregulatory activity of insulin is mitigated during hyperinsulinemia by dampening the efficiency of insulin signaling ("insulin resistance"), this is not the case for most other hormonal actions of insulin, including the promotion of protein synthesis, de novo lipogenesis, and cell proliferation; the inhibition of lipolysis, of autophagy-dependent cellular turnover, and of nuclear factor E2-related factor-2 (Nrf2)-dependent antioxidative; and other defense mechanisms. Hence, there is no general insulin resistance but selective impairment of insulin signaling which causes less glucose uptake from the blood and reduced activation of endothelial NO synthase (eNOS). Because of the largely unrestricted insulin signaling, hyperinsulinemia increases the risk of obesity, type 2 diabetes, and cardiovascular disease and decreases health span and life expectancy. In epidemiological studies, high-dose insulin therapy is associated with an increased risk of cardiovascular disease. Randomized controlled trials of insulin treatment did not observe any effect on disease risk, but these trials only studied low insulin doses up to 40 IU/day. Proof for a causal link between elevated insulin levels and cardiovascular disease risk comes from Mendelian randomization studies comparing individuals with genetically controlled low or high insulin production. Conclusions: The detrimental actions of prolonged high insulin concentrations, seen also in cell culture, argue in favor of a lifestyle that limits circadian insulin levels. The health risks associated with hyperinsulinemia may have implications for treatment regimens used in type 2 diabetes.

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“…Glucose and lipid metabolism are the two major processes involved in increasing the risk and severity of CAD. Abnormal metabolism affects activity of regulatory pathways, composition of the final product, degree of inflammation, and coronary-plaque formation, thus contributing to the development of CAD and accelerating occurrence of adverse cardiovascular events [29,30].…”

Section: Effects On Glucose and Lipid Metabolismmentioning

confidence: 99%

A Review of the Relationship Between CTRP Family and Coronary Artery Disease

Fan

Sun

2020

Curr Atheroscler Rep

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Purpose of Review In recent years, a family of adiponectin paralogs designated as C1q/TNF-related protein (CTRP) has attracted increasing attention. They are inflammatory adipocytokines mostly secreted from epicardial adipose tissue, which modulate the development and prognosis of coronary artery disease (CAD). This review summarizes the pathophysiological roles of individual members of the CTRP superfamily in the development of CAD. Recent Findings Recent studies have revealed how members of the CTRP family, CTRP1, CTRP3, CTRP5, CTRP9, CTRP12, and CTRP13, can influence both development and progression of CAD by modulating metabolic pathways, influencing immuno-inflammatory response, and regulating cardiovascular functions. Summary Research to date has not been sufficient to answer the specific mechanism of the CTRP family in the occurrence and development of CAD. This review explores the evidence of CTRP superfamily regulating different pathophysiology stages of CAD through the immuno-inflammation, glucose and lipid metabolism, and vascular endothelial function.

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Insulin resistance is a cardiovascular risk factor in humans

Cited by 185 publications

References 89 publications

Plasma adiponectin, visfatin, leptin, and resistin levels and the onset of colonic polyps in patients with prediabetes

Plasma adiponectin, visfatin, leptin, and resistin levels and the onset of colonic polyps in patients with prediabetes

Insulin: too much of a good thing is bad

A Review of the Relationship Between CTRP Family and Coronary Artery Disease

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