Relation of fasting insulin related to insertion/deletion polymorphism of angiotensin-converting enzyme-gene and cardiac mass in never-treated patients with systemic hypertension

Potential impact of carbohydrate and fat intake on pathological left ventricular hypertrophy

“…On the other hand, the molecular mechanisms that cause LVH are extremely complex and redundant, and despite significant progress over the last 20 years, the precise signaling pathways remain only partially understood [6][7][8]57,[71][72][73][74][75]. Insulin stimulates protein synthesis and inhibits protein breakdown in the heart [76][77][78], and clinical studies have found that elevated plasma insulin is associated with LVH [23][24][25][26][27][28][29][30]. The dietary intake of carbohydrates (particularly simple sugars) and lipids largely determines the exposure of the heart to insulin and various long chain fatty acid ligands for PPARs, and may play a role in the regulation of cardiomyocyte size under pathological conditions.…”

“…Recent studies demonstrate that cardiomyocyte hypertrophy can also be triggered by activation of insulin signaling pathways [12][13][14], altered adipokine levels [15][16][17][18] or the activity of peroxisome proliferator-activated receptors (PPARs) [19][20][21][22], suggesting that metabolic alterations can play a role in the pathophysiology of LVH. Hypertensive patients with high plasma insulin or metabolic syndrome have a greater occurrence of LVH [23][24][25][26][27][28][29][30], which could be due to insulin activation of the serine-threonine kinase Akt and its downstream targets, resulting in cellular hypertrophy [12,13,31,32]. PPARs also activate cardiac gene expression and growth, and are stimulated by fatty acids [33,34] and consumption of a high fat diet [35][36][37].…”

Effect of interaction between left ventricular dysfunction and endothelial function in hypertension

“…In addition, DD patients are also more prone to develop insulin resistance, which, as previously examined, activates vascular and cardiac growth processes. Accordingly, we recently reported the growth effect of fasting insulin, associated with ACE gene polymorphism, on cardiac mass in a group of previously untreated hypertensive patients [30]. An attractive hypothesis could be that, at least in part, the proliferative effects of angiotensin II are mediated by insulin.…”

“…Previous studies have shown that blood pressure explains only 10% to 25% of the variation in left ventricular mass [25], supporting the hypothesis that other determinants are involved in the cardiac growth in human hypertension. This implies that nonhemodynamic factors, such as sodium-intake [26], genetic [27], or hormonal [28][29][30], contribute to the growth of the heart. In fact, it is well-established that the mechanical forces favoring LVH interact with some potent neurohumoral factors that possess independent stimulatory effects on protein synthesis, interstitial matrix formation, and myofibril size.…”

Association of echocardiographic left ventricular structure with the ACE D/I polymorphism: a meta-analysis

“…[55][56][57][58] All studies combined included 10,320 participants of Asian 25,27,30,33,36,37,39,46,47,49,54,58 (n = 1806; 17.5%), African 27 (n = 16; 0.1%) or Caucasian 16,[21][22][23][24][26][27][28][29]31,32,34,35,38,[40][41][42]44,45,48,[50][51][52][53][55][56][57][59][60][61][62][63] (n = 8498; 82.4%) ethnicity. With respect to blood pressure, 21 studies included only hypertensive patients, [27][28][29]…”