Acute Cardiovascular and Metabolic Effects of Acetate in Men

Abstract

We studied the potential contribution of acetate to the cardiovascular effects of ethanol in 12 healthy male volunteers. Sodium acetate, or sodium chloride in control experiments, was infused i.v. at the rate of 0.033 mEq/kg/min for 60 min. Left ventricular function was examined by M-mode echocardiography and systolic time intervals during infusion and for 60 min thereafter. Blood acetate rose during infusion from 0.19 +/- 0.02 (mean +/- SEM) to a maximum of 0.99 +/- 0.08 mmol/liter. Changes in serum free fatty acids, glycerol, and ketone bodies indicate that acetate inhibited peripheral lipolysis. The volume of urine excreted during the acetate experiment (305 +/- 37 ml) was significantly larger (p less than 0.01) than during the chloride experiment (181 +/- 21 ml). Left ventricular function did not differ between the experiments during the infusions even though at 45 min heart rate was increased by acetate (7%; p less than 0.01, between infusions). After the infusion period, at 75 min the treatment by acetate increased cardiac output from the baseline by 17% (p less than 0.05, between infusions), and decreased peripheral arterial resistance (19%, p less than 0.05), and diastolic blood pressure (10%, p less than 0.01). Circumferential fiber shortening velocity was increased during the acetate experiment maximally by 7% (p less than 0.01) from the baseline at 120 min. These data indicate that acetate is an arterial vasodilator and a mild diuretic and may slightly improve myocardial performance in the concentrations encountered during ethanol metabolism in men.

The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism

“…In isolated adipocytes, acetate and propionate were found to inhibit lipolysis via Ffar2 activation ( 113,114 ). A reduction of lipolysis is consistent with data from human studies where intravenous administration of acetate and propionate reduced plasma free fatty acids and glycerol ( 131,132 ). Ffar2 mediated inhibition of lipolysis is most likely through inactivation of the hormone-sensitive lipase (HSL), which hydrolyzes triglycerides and is one of the key molecules controlling lipolysis in adipose tissue ( 133 ).…”

Short-Chain Fatty Acids Protect Against High-Fat Diet–Induced Obesity via a PPARγ-Dependent Switch From Lipogenesis to Fat Oxidation

“…Such selective PPARg modulators have been proposed by others (55), and our results suggest that SCFAs act as highly effective endogenous selective PPARg modulators. The few human studies that have been conducted showed that intravenous administration of acetate or propionate reduced plasma free fatty acids in humans (56,57), whereas 12 weeks of dietary vinegar (acetate) supplementation in obese subjects led to lower body weight, body fat mass, and serum triglycerides levels than in the placebo-controlled group (16). This makes the inexpensive SCFAs very attractive compounds to prevent and reverse HFD-induced obesity and insulin resistance.…”

Metabolic Homeostasis and Colonic Health: the Critical Role of Short Chain Fatty Acids

“…Given that GPR43 can couple to Gi/o, this suggests that GPR43 in adipocytes may activate the Gi/o pathway to inhibit lipolysis. It is interesting to note that the effects of acetate on reducing plasma FFA levels have been documented in humans [79,80]. Whether these observed effects are mediated through GPR43 and whether activation of GPR43 will lead to suppression of plasma FFA levels need to be further addressed.…”