In abdominally obese men, dietary weight loss targeting a waist circumference of <102 cm improved retinal microvascular caliber, plasma biomarkers of microvascular endothelial function, and the more conventional cardiometabolic risk markers. Aortic stiffness tended to decrease, but FMD was not changed. This trial was registered at clinicaltrials.gov as NCT01675401.

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High Na and low K intakes have adverse effects on blood pressure, which increases the risk for CVD. The role of endothelial dysfunction and inflammation in this pathophysiological process is not yet clear. In a randomised placebo-controlled cross-over study in untreated (pre) hypertensives, we examined the effects of Na and K supplementation on endothelial function and inflammation. During the study period, subjects were provided with a diet that contained 2·4 g/d of Na and 2·3 g/d of K for a 10 460 kJ (2500 kcal) intake. After 1-week run-in, subjects received capsules with supplemental Na (3·0 g/d), supplemental K (2·8 g/d) or placebo, for 4 weeks each, in random order. After each intervention, circulating biomarkers of endothelial function and inflammation were measured. Brachial artery flow-mediated dilation (FMD) and skin microvascular vasomotion were assessed in sub-groups of twenty-two to twenty-four subjects. Of thirty-seven randomised subjects, thirty-six completed the study. Following Na supplementation, serum endothelin-1 was increased by 0·24 pg/ml (95 % CI 0·03, 0·45), but no change was seen in other endothelial or inflammatory biomarkers. FMD and microvascular vasomotion were unaffected by Na supplementation. K supplementation reduced IL-8 levels by 0·28 pg/ml (95 % CI 0·03, 0·53), without affecting other circulating biomarkers. FMD was 1·16 % (95 % CI 0·37, 1·96) higher after K supplementation than after placebo. Microvascular vasomotion was unaffected. In conclusion, a 4-week increase in Na intake increased endothelin-1, but had no effect on other endothelial or inflammatory markers. Increased K intake had a beneficial effect on FMD and possibly IL-8, without affecting other circulating endothelial or inflammatory biomarkers.

Kusters YH, Barrett EJ. Muscle microvasculature's structural and functional specializations facilitate muscle metabolism. Am J Physiol Endocrinol Metab 310: E379-E387, 2016. First published December 29, 2015; doi:10.1152/ajpendo.00443.2015.-We review the evolving findings from studies that examine the relationship between the structural and functional properties of skeletal muscle's vasculature and muscle metabolism. Unique aspects of the organization of the muscle microvasculature are highlighted. We discuss the role of vasomotion at the microscopic level and of flowmotion at the tissue level as modulators of perfusion distribution in muscle. We then consider in some detail how insulin and exercise each modulate muscle perfusion at both the microvascular and whole tissue level. The central role of the vascular endothelial cell in modulating both perfusion and transendothelial insulin and nutrient transport is also reviewed. The relationship between muscle metabolic insulin resistance and the vascular action of insulin in muscle continues to indicate an important role for the microvasculature as a target for insulin action and that impairing insulin's microvascular action significantly affects body glucose metabolism. muscle microvasculature; vasomotion; flowmotion; endothelium; insulin resistance MUSCLE'S MICROVASCULATURE IS THE FINAL INTERFACE through which circulating nutrients, hormones, gases, and electrolytes must pass in journeying to and from the systemic circulation. It has evolved multiple structural and functional adaptations to flexibly and efficiently fulfill its role in optimizing muscle function. Here, we examine how the minute-to-minute metabolic activity of skeletal muscle is coupled to the function of muscle's vasculature. We will discuss how bulk blood flow and flow distribution can regulate nutrient delivery to muscle microvasculature as well as how transendothelial transport processes can modulate the exchange of hormones and metabolites between plasma and the myocytes. We focus on acute regulatory relationships and defer discussion of chronic vascular or myocyte adaptation to environmental, nutritional, and most pathological processes.Muscle blood flow has been measured in numerous classical limb balance and metabolic tracer studies of the acute effects of fasting, feeding, exercise, and hormonal manipulation on muscle nutrient exchange. These methods, however, treat muscle's vasculature as a "black box." Here, we consider muscle microvasculature's specialized architecture and how that architecture might impact nutrient fluxes into and out of the muscle. We will discuss the role of vasomotion and flowmotion in the regulation of microvascular perfusion. We recognize that factors acting on the endothelial cell (EC), the vascular smooth muscle cell (SMC), or pericytes may affect muscle perfusion.We will consider in more detail the effect insulin and exercise have on the endothelium and directly or indirectly on the vascular SMC to influence nutrient delivery.Beyond muscle perfusion, we will co...

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Purpose Sulfur amino acids (SAAs) have been associated with obesity and obesity-related metabolic diseases. We investigated whether plasma SAAs (methionine, total cysteine (tCys), total homocysteine, cystathionine and total glutathione) are related to specific fat depots. Methods We examined cross-sectional subsets from the CODAM cohort (n = 470, 61.3% men, median [IQR]: 67 [61, 71] years) and The Maastricht Study (DMS; n = 371, 53.4% men, 63 [55, 68] years), enriched with (pre)diabetic individuals. SAAs were measured in fasting EDTA plasma with LC–MS/MS. Outcomes comprised BMI, skinfolds, waist circumference (WC), dual-energy X-ray absorptiometry (DXA, DMS), body composition, abdominal subcutaneous and visceral adipose tissues (CODAM: ultrasound, DMS: MRI) and liver fat (estimated, in CODAM, or MRI-derived, in DMS, liver fat percentage and fatty liver disease). Associations were examined with linear or logistic regressions adjusted for relevant confounders with z-standardized primary exposures and outcomes. Results Methionine was associated with all measures of liver fat, e.g., fatty liver disease [CODAM: OR = 1.49 (95% CI 1.19, 1.88); DMS: OR = 1.51 (1.09, 2.14)], but not with other fat depots. tCys was associated with overall obesity, e.g., BMI [CODAM: β = 0.19 (0.09, 0.28); DMS: β = 0.24 (0.14, 0.34)]; peripheral adiposity, e.g., biceps and triceps skinfolds [CODAM: β = 0.15 (0.08, 0.23); DMS: β = 0.20 (0.12, 0.29)]; and central adiposity, e.g., WC [CODAM: β = 0.16 (0.08, 0.25); DMS: β = 0.17 (0.08, 0.27)]. Associations of tCys with VAT and liver fat were inconsistent. Other SAAs were not associated with body fat. Conclusion Plasma concentrations of methionine and tCys showed distinct associations with different fat depots, with similar strengths in the two cohorts.

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