Studie som nevner «alt» om insulinresistens og hva det gjør i kroppen: magefett, symatisk overstimulering, oksidativt stress og blodkardysfunksjon, renin-angiotensin, betennelser og søvnapne.

http://www.nutritionj.com/content/7/1/10

«Visceral obesity, insulin resistance, oxidative stress, endothelial dysfunction, activated renin-angiotensin system, increased inflammatory mediators, and obstructive sleep apnea have been proposed to be possible factors to develop hypertension in the metabolic syndrome. These factors may induce sympathetic overactivity, vasoconstriction, increased intravascular fluid, and decreased vasodilatation, leading to development of hypertension in the metabolic syndrome.»

«As shown in Figure 1, accumulated visceral adipose tissue produce and secrete a number of adipocytokines, such as leptin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), angiotensinogen, and non-esterified fatty acids (NEFA), which induce development of hypertension [11]. «

«Insulin resistance is the main pathophysiologic feature of the metabolic syndrome. Several mechanisms connect insulin resistance with hypertension in the metabolic syndrome. An anti-natriuretic effect of insulin has been established by accumulating data indicating that insulin stimulates renal sodium re-absorption [12–14]. This anti-natriuretic effect is preserved, and may be increased in individuals with insulin resistance, and this effect may play an important role for development of hypertension in the metabolic syndrome [15].»

«NEFA has been reported to raise blood pressure, heart rate, and α1-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance[28]. Insulin resistance increases plasma leptin levels, and leptin has been reported to elevate sympathetic nervous activity, suggesting that leptin-dependent sympathetic nervous activation may contribute to an obesity-associated hypertension [29]. Accumulating data suggest that metabolic syndrome is associated with markers of adrenergic overdrive [30].»

«In rats with the metabolic syndrome, induced by chronic consumption of a high fat, high refined sugar [31], hypertension is associated with oxidative stress [32], avid nitric oxide (NO) inactivation, and down-regulation of NO synthase (NOS) isoforms and endothelial NOS activator[32], suggesting that oxidative stress and endothelial dysfunction may be strongly associated with development of hypertension in the metabolic syndrome. Further, recent evidences suggest that oxidative stress, which is elevated in the metabolic syndrome [33], is associated with sodium retention and salt sensitivity [34].»

«The renin-angiotensin system (RAS) plays a crucial role in blood pressure regulation, by affecting renal function and by modulating vascular tone. The activity of the RAS appears to be regulated by food intake, and overfeeding of rodents has been reported to lead to increased formation of angiotensin II in adipocytes [38]. «

«Recent cohort studies have demonstrated that high-sensitivity C-reactive protein (hsCRP) independently presents additive prognostic values at all levels of metabolic syndrome [45]. Ridker PM, et al. suggest a consideration of adding hsCRP as a clinical criterion for metabolic syndrome[45]. Abnormalities in inflammatory mediators have been also reported to be implicated with development of hypertension.»

«TNF-α is involved in the pathophysiology of hypertension in the metabolic syndrome. TNF-α stimulates the production of endothelin-1 and angiotensinogen [48,49].»

«IL-6 stimulates the central nervous system and sympathetic nervous system, which may result in hypertension [54,55]. The administration of IL-6 leads to elevation in heart rate and serum norepinephrine levels in women [56]. Further, IL-6 induces an increase in plasma angiotensinogen and angiotensin II [57], leading to development of hypertension.»

«Patients with OSA are often considered to be obese, however, Kono M et al. reported that OSA was associated with hypertension, dyslipidemia, and hyperglycemia, independent of visceral obesity [59]. «