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Cited by 99Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesPeroxisome Proliferator-Activated Receptors

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

Begriche, Karima, Massart, Julie, Abbey‐Toby, Adjé, Igoudjil, Anissa, Lettéron, Philippe, Fromenty, Bernard·2008·Obesity
DOI 10.1038/oby.2008.337
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Abstract

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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Authors
Begriche, K., Massart, J., Abbey‐Toby, A., Igoudjil, A., Lettéron, P., & Fromenty, B.
Affiliations
  • Inserm (FR)
  • Hôpital Beaujon (FR)
Corresponding author
Fromenty, Bernard
ORCID
Venue
Obesity
Publisher
Wiley
Published
2008-09
Volume
16
Issue
9
Pages
2053-2067
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
DOI
10.1038/oby.2008.337
OpenAlex
W1967275921
Cited by
99
References
61
Citations by year
2026: 5 · 2025: 7 · 2024: 10 · 2023: 10 · 2022: 5 · 2021: 10 · 2020: 8 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 2 · 2012: 5
FWCI
0.89
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1466 d)
Locations
  • Obesity (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
beta-aminoisobutyric acid, diet-induced obesity, leptin deficiency, ob/ob mice, fatty acid oxidation, hepatic steatosis, liver necroinflammation, impaired glucose tolerance, hypertriglyceridemia, beta-hydroxybutyrate, carnitine palmitoyltransferase 1, de novo lipogenesis, acetyl-CoA carboxylase, leptin secretion, adipose tissue, metabolic disorders
MeSH terms
Alanine Transaminase, Aminoisobutyric Acids, Animals, Antioxidants, Blood Glucose, Body Composition, Cholesterol, Dietary Fats, Fatty Liver, Glucose Tolerance Test, L-Lactate Dehydrogenase, Male, Mice, Inbred C3H, Mice, Obese, Obesity, Triglycerides, Rats, Sprague-Dawley, Leptin, Mice, Rats

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