A RELATIONSHIP BETWEEN IMPAIRED FETAL GROWTH AND REDUCED MUSCLE GLYCOLYSIS REVEALED BY P-31 MAGNETIC-RESONANCE SPECTROSCOPY

Citation
Dj. Taylor et al., A RELATIONSHIP BETWEEN IMPAIRED FETAL GROWTH AND REDUCED MUSCLE GLYCOLYSIS REVEALED BY P-31 MAGNETIC-RESONANCE SPECTROSCOPY, Diabetologia, 38(10), 1995, pp. 1205-1212
Citations number
23
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
0012186X
Volume
38
Issue
10
Year of publication
1995
Pages
1205 - 1212
Database
ISI
SICI code
0012-186X(1995)38:10<1205:ARBIFG>2.0.ZU;2-S
Abstract
Thinness at birth is associated with insulin resistance and an increas ed prevalence of non-insulin-dependent diabetes mellitus in adult life . As muscle is an important site of insulin resistance, and because th in babies have reduced muscle mass, thinness at birth may affect muscl e structure and function and impair carbohydrate metabolism. We have t herefore used P-31 magnetic resonance spectroscopy to investigate the bioenergetics of gastrocnemius and flexor digitorum superficialis musc les in 16 normoglycaemic women who had a low (less than or equal to 23 kg/m(3)) and 9 women who had a high (> 23 kg/m(3)) ponderal index at birth. In the flexor digitorum superficialis study anaerobic metabolis m was stressed with a constant heavy workload. Low ponderal index subj ects fatigued more rapidly (3.3 vs 5.8 min); as phosphocreatine decrea sed, the accompanying drop in muscle pH was less than in the high pond eral index group. In the first minute of exercise phosphocreatine fell and adenosine diphosphate rose more rapidly (p = 0.04 and 0.03, respe ctively). Gastrocnemius showed a similar trend late in exercise (this exercise was more oxidative, becoming more anaerobic with increasing w orkload). These changes were not explained by differences in body comp osition, muscle mass or blood flow. The findings are consistent with a decreased lactic acid and glycolytic adenosine triphosphate productio n in the low ponderal index group and suggest the possibility that the mechanisms which control substrate utilisation and metabolism in adul t life be programmed during prenatal life.