β‐Aminoisobutyric Acid Prevents Diet‐induced Obesity in Mice With Partial Leptin Deficiency

Feb 3, 2009Obesity (Silver Spring, Md.)

Beta-aminoisobutyric acid helps prevent diet-related obesity in mice with reduced leptin

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Abstract

BAIBA (100 mg/kg/day) prevented or limited body fat gain and metabolic disorders in mice partially deficient in leptin fed a high-calorie diet.

BAIBA did not limit obesity or liver fat accumulation in mice completely lacking leptin.
In mice with partial leptin deficiency, BAIBA reduced liver inflammation and improved metabolic markers.
Increased levels of plasma beta-hydroxybutyrate and enhanced fatty acid oxidation were observed with BAIBA treatment.
The treatment resulted in less liver fat synthesis and decreased glucose intolerance in the ob/+ mice.
Leptin levels were restored in plasma, correlating with the reduction of body fat in treated ob/+ mice.
BAIBA stimulated leptin secretion specifically in adipose cells from ob/+ mice but not in those from wild-type mice.

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Beta-Aminoisobutyric acid (BAIBA), a thymine catabolite, increases fatty acid oxidation (FAO) in liver and reduces the gain of body fat mass in Swiss (lean) mice fed a standard chow. We determined whether BAIBA could prevent obesity and related metabolic disorders in different murine models. To this end, BAIBA (100 or 500 mg/kg/day) was administered for 4 months in mice totally deficient in leptin (ob/ob). BAIBA (100 mg/kg/day) was also given for 4 months in wild-type (+/+) mice and mice partially deficient in leptin (ob/+) fed a high-calorie (HC) diet. BAIBA did not limit obesity and hepatic steatosis in ob/ob mice, but reduced liver cytolysis and inflammation. In ob/+ mice fed the HC diet, BAIBA fully prevented, or limited, the gain of body fat, steatosis and necroinflammation, glucose intolerance, and hypertriglyceridemia. Plasma beta-hydroxybutyrate was increased, whereas expression of carnitine palmitoyltransferase-1 was augmented in liver and white adipose tissue. Acetyl-CoA carboxylase was more phosphorylated, and de novo lipogenesis was less induced in liver. These favorable effects of BAIBA in ob/+ mice were associated with a restoration of plasma leptin levels. The reduction of body adiposity afforded by BAIBA was less marked in +/+ mice. Finally, BAIBA significantly stimulated the secretion of leptin in isolated ob/+ adipose cells, but not in +/+ cells. Thus, BAIBA could limit triglyceride accretion in tissues through a leptin-dependent stimulation of FAO. As partial leptin deficiency is not uncommon in the general population, supplementation with BAIBA may help to prevent diet-induced obesity and related metabolic disorders in low leptin secretors.

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β‐Aminoisobutyric Acid Prevents Diet‐induced Obesity in Mice With Partial Leptin Deficiency

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