The Antinatriuretic Effect of Insulin: An Unappreciated Mechanism for Hypertension Associated with Insulin Resistance?

Lozovoy

Arq Bras Endocrinol Metab

et al. 2010

OBJECTIVE: To verify the effects of fish oil and soy on nitric oxide (NO) and blood pressure in patients with metabolic syndrome (MS). SUBJECTS AND METHODS: Sixty women with MS were investigated in a parallel randomized design study. The first group maintained their usual diet; the second group received 25 g/day of soy; the third group received 3 g/day of n-3 fatty acids, and the fourth group the same amount previously cited of n-3 fatty acids and soy. RESULTS: Serum nitric oxide metabolites showed significant increase after 90 days in the fish oil and soy groups. Systolic pressure reduced after 45 days of treatment with fish oil, whereas diastolic pressure decreased significantly throughout the study in the soy group. CONCLUSIONS: NO increase and blood pressure reduction with fish oil or soy protein reinforce the importance of the influence of NO on blood pressure in patients with MS.

Section: Discussionmentioning

confidence: 61%

Nitric oxide enhancement and blood pressure decrease in patients with metabolic syndrome using soy protein or fish oil

Lozovoy

Arq Bras Endocrinol Metab

et al. 2010

“…Insulin is known to activate the sympathetic nervous system 23 and is a potential mediator of sodium retention and volume expansion and, thus, higher BP. [24][25][26][27] Additional prospective studies of adolescents with larger sample size will, nevertheless, be needed to determine the importance of our observation and to delineate underlying mechanisms.…”

Section: Discussionmentioning

confidence: 97%

Influence of High Glycemic Index and Glycemic Load Diets on Blood Pressure During Adolescence

et al. 2012

Abstract-We aimed to prospectively examine the association between the glycemic index and glycemic load of foods consumed and the dietary intakes of carbohydrates, sugars, fiber, and principal carbohydrate-containing food groups (eg, breads, cereals, and sugary drinks) with changes in blood pressure during adolescence. A total of 858 students aged 12 years at baseline (422 girls and 436 boys) were examined from 2004 -2005 to 2009 -2011. Dietary data were assessed from validated semiquantitative food frequency questionnaires. Blood pressure was measured using a standard protocol. In girls, after adjusting for age, ethnicity, parental education, parental history of hypertension, baseline height, baseline blood pressure, change in body mass index, and time spent in physical and sedentary activities, each 1-SD (1-SDϭ7.10 g/d) increase in baseline dietary intake of total fiber was associated with a 0. 2,3 Therefore, preventing elevated BP levels in childhood and adolescence may be an important public health measure to limit the overall disease burden caused by hypertension. 4,5 More recently, there are data to suggest that dietary factors, such as high consumption of carbohydrates, including sugars and soft drinks, could adversely influence BP levels. 6 A recent meta-analysis of intervention studies involving adults 7 shows that diets rich in carbohydrates may be associated with slightly higher BP. In contrast, dietary fiber intake was shown to be inversely associated with BP in adults 8 and with reduced risk of incident cardiovascular disease. 9 To the best of our knowledge, the temporal link between carbohydrate nutrition intake and BP has not been explored in an adolescent population.In addition, previous adult studies have demonstrated a direct association of sugar-sweetened beverage consumption with systolic/diastolic BP and direct associations of fructose and glucose intake with BP. 6,10 In addition, the National Health and Nutrition Examination Survey found that, in a sample of 4867 adolescents aged 12 to 18 years, higher sugar-sweetened beverage consumption was associated with higher serum uric acid levels and systolic BP.11 However, this study had a cross-sectional design, and currently there are no prospective data during adolescence examining this relationship.To better understand the effects of carbohydrate nutrition variables on BP during adolescence, we used data available from a 5-year longitudinal study of adolescents in Australia to determine the following: (1) the association between baseline dietary intakes of total carbohydrate, sugars, glycemic index (GI), glycemic load (GL), and fiber with temporal changes in systolic and diastolic BP and mean arterial BP; (2) the relationship between baseline consumption of soft drinks/ cordials and the principal carbohydrate-containing food groups (eg, breads and cereals, potatoes, and energy-dense nutrient-poor sources of carbohydrates, such as cookies and

American Journal of Physiology-Regulatory, Integrative and Comp

“…Obesity is firmly established as a cause of hypertension, although additional mechanisms besides hyperinsulinemia have been proposed as mechanisms (35,42,56,63). Therefore, it is not surprising that a sodium-retaining action of insulin has continued to be advanced as a contributing factor for sodium retention and hypertension in obesity or metabolic syndrome (53,77,80).…”

Section: Conclusion 1: Insulin Is a Sodium Retainermentioning

confidence: 99%

Sodium-retaining effect of insulin in diabetes

Brands¹,

Manhiani²

2012

Brands MW, Manhiani MM. Sodium-retaining effect of insulin in diabetes. Am J Physiol Regul Integr Comp Physiol 303: R1101-R1109, 2012. First published October 3, 2012 doi:10.1152/ajpregu.00390.2012.-Insulin has long been hypothesized to cause sodium retention, potentially of enough magnitude to contribute to hypertension in obesity, metabolic syndrome, and Type II diabetes. There is an abundance of supportive evidence from correlational analyses in humans, acute insulin infusion studies in humans and animals, and chronic insulin infusion studies in rats. However, the absence of hypertension in human insulinoma patients, and negative results for sodium-retaining or blood pressure effects of chronic insulin infusion in a whole series of dog studies, strongly refute the insulin hypothesis. We recently questioned whether the euglycemic, hyperinsulinemia model used for most insulin infusion studies, including the previous chronic dog studies, was the most appropriate model to test the renal actions of insulin in obesity, metabolic syndrome, and Type II diabetes. In those circumstances, hyperinsulinemia coexists with hyperglycemia. Therefore, we tested the sodium-retaining effect of insulin in chronically instrumented, alloxan-treated diabetic dogs. We used 24 h/day intravenous insulin infusion to regulate plasma insulin concentration. Induction of diabetes (ϳ400 mg/dl) caused sustained natriuresis and diuresis. However, if we clamped insulin at baseline, control levels, i.e., prevented it from decreasing, then the sustained natriuresis and diuresis were completely reversed, despite the same level of hyperglycemia. We also found that 24 h/day intrarenal insulin infusion had the same effect in diabetic dogs but had no sodium-retaining action in normal dogs. This new evidence that insulin has a sodium-retaining effect during hyperglycemia may have implications for maintaining sodium balance in uncontrolled Type II diabetes.diabetes; insulin; diuresis; natriuresis; sodium balance RAISING THE QUESTION of whether insulin causes renal sodium retention, either in a scientific presentation or in the literature, immediately evokes one of two responses from the audience: 1) "I already know that insulin causes sodium retention", or 2) "Insulin does not cause sodium retention." Those maintaining the latter essentially have closed the book on the subject, and those holding to the former are interested in mechanisms but not the overarching question of whether insulin causes renal sodium retention. There is a wealth of literature to support both positions. However, nuances in many early studies raised issues that never were resolved. Inertia in the literature left many of those issues fading in the distance, all but erased from current thinking. We recently revisited the question about insulin and sodium retention, and our results were so striking that both positions on the subject warrant reconsideration. This review will chronologically present the literature supporting each position and show how our recent reports add new insigh...