The insulin-like growth factor I system: Physiological and pathophysiological implication in cardiovascular diseases associated with metabolic syndrome

Ren, Jun; Anversa, Piero

doi:10.1016/j.bcp.2014.12.006

Cited by 87 publications

(64 citation statements)

References 126 publications

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“…We here observed that rats fed with a diet enriched with Bio-Oil Spread showed reduced anthropometric index, in particular abdominal fat, with respect to HFD-fed animals. As largely shown in animal models and in humans, these parameters are closely associated with dyslipidemia, disorders in glucose metabolism, and severe cardiovascular dysfunctions, which remarkably enhance the risk of myocardial infarction [27,35,36]. Consistent with these metabolic alterations, we found in HFD rats a lipid profile indicative of dyslipidemia.…”

Section: Discussionsupporting

confidence: 83%

“…In addition, IGF1R, an established factor in cardiac hypertrophy, is overexpressed in hypertrophic heart mediating the hypertrophic pathology process. In particular, it has been shown that the short-term activation of IGF signaling pathway promotes physiologic growth, whereas sustained hyperactivation leads to the development of pathologic hypertrophy and HF [36,37]. Interestingly, we observed that the expression of IGF-1R and myocardial hypertrophy in SD heart, are lower than those of HDF heart, suggesting that SD diet protects the heart from obesity dependent hypertrophy.…”

Section: Discussionmentioning

confidence: 56%

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The innovative “Bio-Oil Spread” prevents metabolic disorders and mediates preconditioning-like cardioprotection in rats

Quintieri

Filice

Amelio

et al. 2016

Nutrition, Metabolism and Cardiovascular Diseases

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Background and aims: Obesity is often associated with an increased cardiovascular risk. The food industry and the associated research activities focus on formulating products that are a perfect mix between an adequate fat content and health. We evaluated whether a diet enriched with Bio-Oil Spread (SD), an olive oil-based innovative food, is cardioprotective in the presence of high-fat diet (HFD)-dependent obesity.Methods and Results: Rats were fed for 16 weeks with normolipidic diet (ND; fat: 6.2%), HFD (fat: 42%), and ND enriched with SD (6.2% of fat þ 35.8% of SD). Metabolic and anthropometric parameters were measured. Heart and liver structures were analyzed by histochemical examination. Ischemic susceptibility was evaluated on isolated and Langendorff-perfused cardiac preparations. Signaling was assessed by Western blotting. Compared to ND rats, HFD rats showed increased body weight and abdominal obesity, dyslipidemia, and impaired glucose tolerance. Morphological analyses showed that HFD is associated with heart and liver modifications (hypertrophy and steatosis, respectively), lesser evident in the SD group, together with metabolic and anthropometric alterations. In particular, IGF-1R immunodetection revealed a reduction of hypertrophy in SD heart sections. Notably, SD diet significantly reduced myocardial susceptibility against ischemia/reperfusion (I/R) with respect to HFD through the activation of survival signals (Akt, ERK1/2, and Bcl2). Systolic and diastolic performance was preserved in the SD group. Conclusions: We suggest that SD may contribute to the prevention of metabolic disorders and cardiovascular alterations typical of severe obesity induced by an HFD, including the increased ischemic susceptibility of the myocardium. Our results pave the way to evaluate the introduction of SD in human alimentary guidelines as a strategy to reduce saturated fat intake. IntroductionMen and women of all ages, races, and ethnic groups can be affected by obesity [1] and this is often accompanied by an increased morbidity and mortality due an increase of cardiovascular disease (CVD) risk factors [2,3]. Severe obesity causes permanent hemodynamic alterations that progressively impair cardiac structure and function. When comorbidities (i.e., systemic hypertension, sleep apnea, and hypoventilation) are present together with obesity, cardiac alterations progress to heart failure (HF) [4]. Metabolic syndrome (MetS) is a condition in which a high CVD risk is associated with obesity. It is characterized by disturbed glucose homeostasis, dyslipidemia, and hypertension [5] and is established in the presence of three of the following parameters: (i) waist circumference >40 (men) and >35 (women) inches; (ii) triglycerides >150 mg/dl; (iii) HDL (high-density lipoprotein) cholesterol <40 (men) and <50 (women) mg/dl; (iv) blood pressure >130/85 mm Hg; and (v) fasting glucose >100 mg/dl [6]. Currently, nutritional therapy is regarded as the best practice to prevent and/or reduce the cardiovascular damages associated ...

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 56%

The innovative “Bio-Oil Spread” prevents metabolic disorders and mediates preconditioning-like cardioprotection in rats

Quintieri

Filice

Amelio

et al. 2016

Nutrition, Metabolism and Cardiovascular Diseases

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“…As shown previously, acute inhibition of insulin receptor partially impairs glucose tolerance in BAT transplant recipients, indicating a direct action of IGF-I in glucose metabolism (27). Recent studies show that metabolic disease is associated with subnormal IGF-I levels and that diet-induced reversal of T2D is accompanied by an increase in IGF-I levels (20,54).…”

Section: Discussionmentioning

confidence: 67%

“…3 and 5). Several studies show that metabolic disease is associated with decrease in IGF-I levels, whereas the underlying mechanisms are not yet known (54).…”

Section: Resultsmentioning

confidence: 99%

Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

Gunawardana

Piston

2015

American Journal of Physiology-Endocrinology and Metabolism

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Gunawardana SC, Piston DW. Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant. Am J Physiol Endocrinol Metab 308: E1043-E1055, 2015. First published April 21, 2015; doi:10.1152/ajpendo.00570.2014.-Traditional therapies for type 1 diabetes (T1D) involve insulin replacement or islet/pancreas transplantation and have numerous limitations. Our previous work demonstrated the ability of embryonic brown adipose tissue (BAT) transplants to establish normoglycemia without insulin in chemically induced models of insulin-deficient diabetes. The current study sought to extend the technique to an autoimmune-mediated T1D model and document the underlying mechanisms. In nonobese diabetic (NOD) mice, BAT transplants result in complete reversal of T1D associated with rapid and longlasting euglycemia. In addition, BAT transplants placed prior to the onset of diabetes on NOD mice can prevent or significantly delay the onset of diabetes. As with streptozotocin (STZ)-diabetic models, euglycemia is independent of insulin and strongly correlates with decrease of inflammation and increase of adipokines. Plasma insulinlike growth factor-I (IGF-I) is the first hormone to increase following BAT transplants. Adipose tissue of transplant recipients consistently express IGF-I compared with little or no expression in controls, and plasma IGF-I levels show a direct negative correlation with glucose, glucagon, and inflammatory cytokines. Adipogenic and anti-inflammatory properties of IGF-I may stimulate regeneration of new healthy white adipose tissue, which in turn secretes hypoglycemic adipokines that substitute for insulin. IGF-I can also directly decrease blood glucose through activating insulin receptor. These data demonstrate the potential for insulin-independent reversal of autoimmune-induced T1D with BAT transplants and implicate IGF-I as a likely mediator in the resulting equilibrium. type 1 diabetes; brown adipose tissue; insulin independent; transplantation; insulin-like growth factor I TYPE 1 DIABETES (T1D) is characterized by autoimmune-mediated destruction of pancreatic ␤-cells, resulting in absolute deficiency of insulin and loss of glycemic control. Treatments for T1D, despite having been refined over many years, are geared mainly toward replacing insulin, which involves numerous risks and limitations. Direct insulin replacement via daily injections or insulin pump does not cure the disease and requires life-long repeated administration. In addition to the inconvenience, direct insulin therapy requires careful monitoring of dosage and blood glucose levels and can lead to potentially fatal hypoglycemic episodes. Pancreas transplantation, the only available treatment with a good chance of long-term insulin independence, requires invasive surgery and life-long immunosuppressive therapy. Islet transplantation, although less invasive, is limited by the availability of donor tissue and the need for immunosuppression, and patients often return to insulin dependence in the long...

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“…Accumulating evidence supports the regulatory roles of IGF-1 in proliferation, differentiation, metabolism, senescence, and apoptosis (14). The mitogen-activated protein kinase (MAPK) cascade and the phosphatidylinositol 3'-kinase (PI3K) pathway are involved in the mitogenic action and the metabolic and antiapoptotic signals of IGF-1 (15). In humans, an inverse association between circulating IGF-1 levels and atherosclerotic cardiovascular diseases as well as the prevalence of metabolic syndrome and its components has been observed (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

The correlation between insulin-like growth factor 1 (IGF-1) and novel adipocytokines in postmenopausal women: A population-based study

et al. 2017

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The adipocytokines and insulin-like growth factor 1 (IGF-1) are involved in insulin resistance, the cardiometabolic syndrome, and atherosclerosis. Therefore, investigating the relationship between circulating levels of the novel adipocytokines and IGF-1 is worthwhile. The correlation between IGF-1, visfatin, and omentin-1 has not been adequately investigated. In a population-based study, 324 postmenopausal women were randomly selected. Circulating IGF-1, visfatin, omentin-1, adiponectin, and high-sensitivity C-reactive protein (hs-CRP) levels were measured with the highly specific enzyme-linked immunosorbent assay method. In multiple regression analyses adjusted for alkaline phosphatase, osteocalcin, and hs-CRP, circulating IGF-1 was significantly correlated with visfatin levels (standardized β coefficient [β] = 0.13, partial correlation coefficient [r] = 0.12, p = 0.028). The significant positive correlation between serum IGF-1 and visfatin levels remained after additional adjustments for age and BMI (β = 0.12, r = 0.12, p = 0.025), metabolic syndrome (β = 0.13, r = 0.12, p = 0.021), and type 2 diabetes mellitus (β = 0.13, r = 0.12, p = 0.026). No significant correlations were found between IGF-1, adiponectin, and omentin-1. There is a significant correlation between serum IGF-1 and visfatin levels in postmenopausal women beyond metabolic syndrome, type 2 diabetes, bone formation markers, and hs-CRP levels. The observed correlation between higher circulating IGF-1 and the higher visfatin levels might be a physiological compensation and adaptation to protect against visfatin-induced proinflammatory effects. ARTICLE HISTORY

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The insulin-like growth factor I system: Physiological and pathophysiological implication in cardiovascular diseases associated with metabolic syndrome

Cited by 87 publications

References 126 publications

The innovative “Bio-Oil Spread” prevents metabolic disorders and mediates preconditioning-like cardioprotection in rats

The innovative “Bio-Oil Spread” prevents metabolic disorders and mediates preconditioning-like cardioprotection in rats

Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

The correlation between insulin-like growth factor 1 (IGF-1) and novel adipocytokines in postmenopausal women: A population-based study

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