IntroductionWe evaluated the relationship between adipokine plasma concentrations and
body fat distribution and the metabolic syndrome.MethodsIn a cohort of 1215 patients with clinically manifest vascular disease the
relation between subcutaneous adipose tissue, visceral adipose tissue, waist
circumference, body mass index and plasma concentrations of adipsin,
chemerin, monocyte chemoattractant protein-1, migration inhibitory factor,
nerve growth factor, resistin, plasma amyloid A1, adiponectin, leptin,
plasminogen activator inhibitor-1 and hepatic growth factor were
cross-sectionally assessed with linear regression and adjusted for age and
gender. The relation between adipokines and the metabolic syndrome was
cross-sectionally evaluated using logistic regression. An adipokine profile
was developed to measure the effect of combined rather than single
adipokines.ResultsAdiposity was related to higher nerve growth factor, hepatic growth factor,
migration inhibitory factor, leptin and adipsin and with lower chemerin,
plasminogen activator inhibitor-1, resistin, plasma amyloid A1 and
adiponectin. The strongest positive relations were between body mass index
and adipsin (β 0.247; 95% CI 0.137–0.356) and leptin (β 0.266; 95% CI
0.207–0.324); the strongest negative relations were between body mass index
and plasma amyloid A1 (β –0.266; 95% CI –0.386 to –0.146) and visceral
adipose tissue and adiponectin (β –0.168; 95% CI –0.226 to –0.111). There
was no relation between subcutaneous adipose tissue and adipokines. Odds for
the metabolic syndrome were higher with each 1 SD higher hepatic growth
factor (OR 1.21; 95% CI 1.06–1.38) and leptin (OR 1.26; 95% CI 1.10–1.45)
and lower with each 1 SD higher adiponectin (OR 0.73; 95% CI 0.64–0.83) and
resistin (OR 0.85; 95% CI 0.74–0.97). The adipokine profile was related to
the metabolic syndrome (OR 1.03; 95% CI 1.00–1.06).ConclusionPlasma concentrations of adipokines are related to obesity and body fat
distribution. The relation between adipokine concentrations and the
metabolic syndrome is independent of visceral adipose tissue.
Renin inhibition, but not sympathoinhibition or diuretic therapy, improves endothelial function and results in larger reductions of 24-h, office, and central blood pressure in obesity-related hypertension. This adds weight to the hypothesis that inhibition of the renin-angiotensin-aldosterone system is an effective first step in the treatment of obesity-related hypertension.
Adipose tissue dysfunction is defined as an imbalance between pro-and anti-inflammatory adipokines, causing insulin resistance, systemic low-grade inflammation, hypercoagulability, and elevated blood pressure. These can lead to cardiovascular disease and diabetes mellitus type 2. Although quantity of adipose tissue is an important determinant of adipose tissue dysfunction, it can be diagnosed in both obese and lean individuals. This implies that not only quantity of adipose
(1)H-MRS is a feasible and reproducible method for FFA profiling in abdominal adipose tissue in abdominally obese individuals. (1)H-MRS has potential as diagnostic tool for noninvasive identification of adipose tissue dysfunction.
BackgroundIn patients with obesity-related hypertension (ORH), reaction to antihypertensive medication is likely influenced by patientcharacteristics.MethodsEffects of aliskiren, moxonidine and hydrochlorothiazide on 24-h blood pressure (BP) were compared to placebo. Linear mixed effect models were used to analyze the effect of patient characteristics on BP levels and treatment response.ResultsSystolic BP response to aliskiren was higher in patients with a BMI > 30.7 kg/m2 compared to patients with a BMI ≤ 30.7 kg/m2 (−21 mmHg versus -4 mmHg). In patients with a hsCRP > 1.8 mg/L the systolic BP response to aliskiren was higher than in patients with a low hsCRP (−15 mmHg versus −7 mmHg). Hydrochlorothiazide (HCTZ) treatment effect on systolic BP was −13 mmHg when heart rate > 71 beats/min compared to -3 mmHg when heart rate was ≤ 71 beats/min.ConclusionIn patients with ORH, BP response to aliskiren is positively related to BMI and hsCRP. Systolic BP response to HCTZ is positively related to heart rate and negatively to renin levels.Trial registration
NCT01138423. Registered June 4th, 2010.
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