Effect of weight loss on lactate transporter expression in skeletal muscle of obese subjects.
The effects of weight loss on skeletal muscle lactate transporter [monocarboxylate transporter (MCT)] expression in obese subjects were investigated to better understand how lactate transporter metabolism is regulated in insulin-resistant states. Ten obese subjects underwent non-macronutrient-specific energy restriction for 15 wk. Anthropometric measurements and a needle biopsy of the vastus lateralis muscle before and after the weight loss program were performed. Enzymatic activity, fiber type distribution, and skeletal muscle MCT protein expression were measured. Muscle from nonobese control subjects was used for comparison of MCT levels. The program induced a weight loss of 9.2 +/- 1.6 kg. Compared with controls, muscle from obese subjects showed a strong tendency (P = 0.06) for elevated MCT4 expression (+69%) before the weight loss program. MCT4 expression decreased (-7%) following weight loss to reach levels that were not statistically different from control levels. There were no differences in MCT1 expression between controls and obese subjects before and after weight loss. A highly predictive regression model (R2 = 0.93), including waist circumference, citrate synthase activity, and percentage of type 1 fibers, was found to explain the highly variable MCT1 response to weight loss in the obese group. Therefore, in obesity, MCT1 expression appears linked both to changes in oxidative parameters and to changes in visceral adipose tissue content. The strong tendency for elevated expression of muscle MCT4 could reflect the need to release greater amounts of muscle lactate in the obese state, a situation that would be normalized with weight loss as indicated by decreased MCT4 levels.
Metz
Lore
L
Département de Physiologie des Interactions EA 701 Muscles et Pathologies chroniques, Institut de biologie, Montpellier, France.
Mercier
Jacques
J
Tremblay
Angelo
A
Alméras
Natalie
N
Joanisse
Denis R
DR
D000328:Adult; D019440:Anti-Obesity Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D031204:Caloric Restriction; D002950:Citrate (si)-Synthase / Q000378:metabolism; D005260:Female; D005277:Fenfluramine / Q000627:therapeutic use*; D005951:Glucose Tolerance Test; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D027501:Monocarboxylic Acid Transporters / Q000378:metabolism*; D018657:Muscle Fibers, Slow-Twitch / Q000378:metabolism; D009124:Muscle Proteins / Q000378:metabolism; D009765:Obesity / Q000178:diet therapy / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D052097:Quadriceps Muscle / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D027981:Symporters / Q000378:metabolism; D016896:Treatment Outcome; D015431:Weight Loss; D000099233:Monocarboxylate Transport Protein 1
D019440:Anti-Obesity Agents; D001786:Blood Glucose; D002950:Citrate (si)-Synthase; D005277:Fenfluramine; D007770:L-Lactate Dehydrogenase; D019344:Lactic Acid; D027501:Monocarboxylic Acid Transporters; D009124:Muscle Proteins; D027981:Symporters; D000099233:Monocarboxylate Transport Protein 1; C406962:SLC16A4 protein, human