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Moderate Caloric Restriction, But Not Physiological Hyperleptinemia Per Se, Enhances Mitochondrial Oxidative Capacity in Rat Liver and Skeletal Muscle—Tissue-Specific Impact on Tissue Triglyceride Content and AKT Activation

Clinica Medica (R.B., M.Z., A.B., G.B., L.V.-S., G.G.), Department of Clinical, Morphological and Technological Sciences, and Centro Servizi Polivalenti di Ateneo (CSPA)-Animal Facility (M.S.), University of Trieste, Trieste 34100, Italy

Address all correspondence and requests for reprints to: Rocco Barazzoni, M.D., Ph.D., Clinica Medica, University of Trieste, Ospedale Cattinara, Strada di Fiume 447, 34100 Trieste, Italy. E-mail: barazzon{at}units.it.

The study aimed at determining, in lean tissues from nonobese rats, whether physiological hyperleptinemia with leptin-induced reduced caloric intake and/or calorie restriction (CR) per se: 1) enhance mitochondrial-energy metabolism gene transcript levels and oxidative capacity; and 2) reduce triglyceride content. Liver and skeletal muscles were collected from 6-month-old Fischer 344 rats after 1-wk leptin sc infusion (0.4 mg/kg · d: leptin + 3-fold leptinemia vs. ad libitum-fed control) or moderate CR (–26% of those fed ad libitum) in pair-fed animals (CR). After 1 wk: 1) leptin and CR comparably enhanced transcriptional expression of mixed muscle mitochondrial genes (P < 0.05 vs. control); 2) CR independently increased (P < 0.05 vs. leptin-control) hepatic mitochondrial-lipooxidative gene expression and oxidative capacity; 3) hepatic but not muscle mitochondrial effects of CR were associated (P < 0.01) with increased activated insulin signaling at AKT level (P < 0.05 vs. leptin-control); 4) liver and muscle triglyceride content were comparable in all groups. In additional experiments, assessing time course of posttranscriptional CR effects, 3-wk superimposable CR (P < 0.05): 1) increased both liver and muscle mitochondrial oxidative capacity; and 2) selectively reduced muscle triglyceride content. Thus, in nonobese adult rat: 1) moderate CR induces early increments of mitochondrial-lipooxidative gene expression and time-dependent increments of oxidative capacity in liver and mixed muscle; 2) sustained moderate CR alters tissue lipid distribution reducing muscle but not liver triglycerides; 3) mitochondrial-lipid metabolism changes are tissue-specifically associated with hepatic AKT activation; 4) short-term physiological hyperleptinemia has no independent stimulatory effects on muscle and liver mitochondrial-lipooxidative gene expression. Increased lean tissue oxidative capacity could favor substrate oxidation over storage during reduced nutrient availability.

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