Hyperinsulinemia refers to an elevated level of circulating insulin (80 and 100 µU/mL), often leading to metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (T2D). There is no precise and universally accepted definition of hyperinsulinemia and insulin resistance. The literature in the field remains unclear regarding whether insulin resistance precedes the development of hyperinsulinemia. Recently, a new hypothesis has been proposed suggesting that chronic hyperinsulinemia precedes and causes insulin resistance. The causes of the initiation of hyperinsulinemia, insulin resistance, and type 2 diabetes are multifactorial. Thus, it is not easy to define in general. Recent work demonstrates that the main prediabetic factor leading to insulin resistance is chronic hyperinsulinemia. However, recent work in the literature proposes that relatively long-term hyperinsulinemia does precede insulin resistance and already promotes cardiovascular remodeling. This later may lead to the development of vascular diseases such as hypertension. Thus, defining hyperinsulinemia and insulin resistance, as well as their signaling pathways implicated in the development of type 2 diabetes (T2D), needs to be clarified.

Our knowledge on essential hypertension is vast, and its treatment is well known. Not all hypertensives are salt-sensitive. The available evidence suggests that even normotensive individuals are at high cardiovascular risk and lower survival rate, as blood pressure eventually rises later in life with a high salt diet. In addition, little is known about high sodium (Na⁺) salt diet-sensitive hypertension. There is no doubt that direct and indirect Na⁺ transporters, such as the Na/Ca exchanger and the Na/H exchanger, and the Na/K pump could be implicated in the development of high salt-induced hypertension in humans. These mechanisms could be involved following the destruction of the cell membrane glycocalyx and changes in vascular endothelial and smooth muscle cells membranes’ permeability and osmolarity. Thus, it is vital to determine the membrane and intracellular mechanisms implicated in this type of hypertension and its treatment.

Although insulin-induced cardiac hypertrophy is reported, very little information is available on the hypertrophic effect of insulin on ventricular cardiomyocytes and the regulation of sodium and calcium homeostasis. Taurine is a non-essential amino acid synthesized by cardiomyocytes and the brain and is present in low quantities in many foods, particularly seafood. The purpose of this study was to investigate whether chronic exposure to insulin induces hypertrophy of ventricular cardiomyocytes that are associated with changes in Na⁺ and Ca²⁺ homeostasis and whether taurine pre-treatment prevents these effects. Our results showed that chronic treatment with insulin leads to cardiomyocyte hypertrophy that is associated with an increase in basal intracellular Na⁺ and Ca²⁺ levels. Furthermore, long-term taurine treatment prevents morphological and ionic remodeling induced by insulin. In addition, blocking the Na⁺-taurine co-transporter prevented the taurine antihypertrophic effect. Finally, the insulin-induced remodeling of cardiomyocytes was associated with a decrease in the ratio of phospho-CREB (pCREB) to total cAMP response element binding protein (CREB); taurine prevented this effect. In conclusion, our results show that insulin induces ventricular cardiomyocyte hypertrophy via downregulation of the pCREB/tCREB level and that chronic taurine treatment prevents this effect.

Premature death due to heart failure is a major health problem. Taurine is a non-essential amino acid that has received much attention. However, although many studies have been carried out on the beneficial effects of taurine in cardiac pathophysiology, no studies have investigated the effect of taurine treatment on the development of hereditary cardiomyopathy (HCM) associated with hypertrophy, heart failure, and early death. This study aims to verify whether short-term treatment (20 days) with taurine in tap water prevents the development of hypertrophy and premature death in hereditary cardiomyopathy of the hamster (HCMH) of the line UM-X7.1 and if its effect is sex-dependent. Our results show that treatment for 20 days with taurine (250 mg/kg/day or 25 mg/animal/day) during the development of the hypertrophic phase (220 days old) significantly decreased (p < 0.01) the heart weight to body weight ratio in male HCMHs without affecting the female. During the 20 days (220–240 days old), there were nearly 40% premature deaths in non-treated males HCMHs and 50% in female HCMHs. Treatment for 20 days wholly and significantly prevented early death in both males and females HCMHs. Our results demonstrate that short-term treatment with taurine prevents the development of cardiac hypertrophy associated with HCM in a sex-dependent manner; however, it prevents early death in a sex-independent fashion. Our results suggest that taurine supplementation could be used to treat HCM.

Elevated circulating insulin levels between 80 and 100 µU/mL characterize hyperinsulinemia, which often leads to metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (T2D). Elevated circulating insulin levels can directly affect vascular function and contribute to the pathophysiology of the cardiovascular system, including secondary arterial hypertension (SAH) and atherosclerosis. It is well known that hyperinsulinemia induced remodeling of the heart. However, there is no information on whether intrinsic differences exist between human vascular smooth muscle cells (VSMCs) and if in vitro mimicking hyperinsulinemia induces human VSMCs morphological and intracellular homeostasis remodeling in a sex- and sex hormones-dependent manner. Our in vitro cultured human VSMCs, coupled with quantitative 3D confocal imaging results, show that intrinsic differences exist between VSMCs from young men and women. Chronic hyperinsulinemia (80 µU/mL, 48 h treatment) increases cell and nuclear volumes associated with increased intracellular calcium (Ca²⁺) and ROS and decreased glutathione. In the absence of hyperinsulinemia, pretreatment with testosterone in VSMCs from men and oestradiol in VSMCs from women had no effect. Both sex hormones partially but not completely prevented hyperinsulinemia-induced remodeling of VSMCs from young men and women. The increase in VSMC volume may increase the thickness of the tunica media, leading to a decrease in the lumen of the blood vessel, which promotes the development of SAH and atherosclerosis in a sex-dependent manner.

Generation of reactive oxygen species (ROS) is a physiological product of cell activity that is mainly generated by the mitochondria as well as by transmembrane NADPH oxidases (NOX1–5) present at the plasma and nuclear envelope membranes. The level of basal intracellular ROS is regulated by endogenous antioxidants such as glutathione (GSH), and the endogenous and exogenous antioxidant taurine. These two antioxidants are present in all types of cells and more particularly in the heart and the vascular system. They regulate and control intrcellular normal ROS levels in order to prevent an increase that induces dysfunction of the cardiovascular system. There are also exogenous antioxidants that are present in many types of food such as vitamin C, vitamin E, and resveratrol. These exogenous antioxidants are necessary to complement the effect of endogenous antioxidants. However, according to the literature, it is difficult to generalize about the beneficial effect of exogenous antioxidants in preventing cardiovascular disease. This does not necessarily seem to be the case for endogenous antioxidants. In this review, we will discuss the advantages and disadvantages of using exogenous and endogenous antioxidants, and suggest the potential application of one of them.