engleski

Visceral Fat, Vitamin D and RAAS Powerplay; from Obesity to Hypertension

The prevalence of obesity and hypertension is increasing worldwide. Since there is strong evidence that the prevalence of hypertension increases sharply with increasing body weight, in this lecture I will address some pathophysiological consideration and present data from my own studies. First topic is visceral fat. The exact mechanism by which excess of visceral fat induces hypertension remains poorly understood. One of the possible answers is increased immune cell infiltration, inflammation, and secretion of vasoconstrictor mediators. A total of 54 obese participants (Group 1 with hypertension, Group 2 without hypertension) were compared with 14 healthy normal weight participants. Body composition was estimated by bioelectrical impedance analysis. Data showed positive correlation between body mass index (BMI) and body fat mass in Group 1 (r=0, 93) and Group 2 (r=0, 69), however it was shown that obese patients with hypertension have significantly more visceral fat mass (P<0.01). Body composition and obesity are leading to the second topic, vitamin D. Observational studies find an inverse relationship between plasma 25-hydroxyvitamin D concentration and obesity. To evaluate this issue, 33 obese patients (Group 1 with hypertension, Group 2 without hypertension) were analyzed. Secondary causes of obesity were excluded, and no participant took vitamin D supplements. Again, body composition was estimated. There was no significant difference between low vitamin D in both groups (40 vs. 36 nmol/L). In Group 1, vitamin D level positively correlated with muscle mass (r = 0.68) ; this correlation was insignificant in Group 2. Sarcopenic obesity is a unique clinical condition where low bone and muscle mass coexist in individuals with obesity. Alterations in adipose tissue, skeletal muscle and bone are strictly interconnected, and vitamin D plays key roles in several metabolic pathways. Also, vitamin D plays an important role in suppressing renin–angiotensin–aldosterone system (RAAS) and decreasing blood pressure which leads to the last topic. It is well known that glucagon-like peptide-1 (GLP-1) has many effects on the human body ; glucose and weight lowering effect are used in pharmacotherapy. The antihypertensive and renoprotective effects of GLP-1 receptor agonists are partly explained by their vasoactive effect and increased natriuresis, but their positive influences on blood pressure and the development and progression of kidney diseases are attributed to many unknown effects. In the study 14 healthy participants (after overnight fasting and oral sodium loading) were randomly assigned to receive either placebo (500 ml of 0.9% saline) or GLP-1 infusion (1.5 pmol/kg/min dissolved in 500 ml of 0.9% saline) over a 3-h period. After 7 days, the protocol was repeated (those receiving placebo got GLP-1 and vice versa). It was confirmed that three hours after GLP-1 infusion, aldosterone decreased significantly (p < 0.008). This study showed that native GLP-1 can decrease aldosterone secretion in a group of healthy individuals, supporting the idea of beneficial outcomes of GLP-1 on blood pressure and the RAAS. Knowing that GLP- plays an important role in fat distribution takes us back to the first topic.

Visceral Fat ; Vitamin D ; RAAS ; Obesity ; Hypertension

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