The anabolic actions of growth hormone and thyroxine on protein metabolism in Snell dwarf and normal mice

Abstract

The individual effects of GH and thyroxine (T4) on protein metabolism were determined in dwarf and normal mice in vivo. The hormone deficiencies of dwarf mice (low serum concentrations of GH and T4) resulted in decreased protein synthesis rates in skeletal muscle and liver, but no difference in synthesis rates in heart. The efficiency of synthesis (g protein/g RNA per day; KRNA) was lower in all three tissues in dwarf compared with normal mice, but effects on RNA concentration were not consistent; there was no change in muscle, a decrease in liver and an increase in heart. Treatment of dwarf mice for 9 days with either human GH or T4 caused increases in body weight and length. Protein synthesis rates were increased in muscle, liver and heart by either hormone, though much more so with T4 than GH. In muscle and liver both GH and T4 treatment resulted in an increased RNA concentration, but T4 treatment also increased KRNA. In heart, both GH and T4 increased KRNA with no change in RNA concentration. GH caused no significant changes in protein degradation rates so that growth rates were increased. T4 increased degradation rates so that there was no increased net growth in muscle or liver; in heart, T4 did induce increased growth despite the large increase in degradation rate. Tibial length was increased by both hormones; GH treatment of dwarf mice also increased cartilage sulphate incorporation on day 9, but T4 treatment did not, suggesting that bone growth is transient with T4 treatment. Normal mice showed no changes in growth or tissue protein metabolism in response to GH, but following T4 treatment there was increased protein turnover due to higher tissue RNA concentrations, although only heart growth was increased. Thus normal mice showed almost no net response to GH or T4, but dwarf mice showed a large response to both hormones. The response was different, however, in that GH caused concomitant increases in growth rates whereas T4 altered body tissue proportions.

The sodium pump and other mechanisms of thermogenesis in selected tissues

“…Contributions of hepatic protein synthesis to hepatic 0 2 consumption are available in the literature for a variety of species (Table 3) and are affected by physiological manipulation. Similarly, the gastrointestinal tract contributes substantially to wholebody 0 2 utilization (Huntington & McBride, 1988), and even though it only amounts to Thyroidectomy decreases the FSR of skeletal muscle in rats (Brown & Millward, 1983) whereas T3 treatment of mice or rats increases rates of protein synthesis (Carter et al 1982;Bates & Holder, 1988;Jepson et al 1988) (see Table 4). The study of Jepson et al (1988) indicated a significant linear relationship between the rate of muscle protein synthesis and T3 treatment.…”

Aging and TOR: interwoven in the fabric of life

“…In 1973, Korner [73] argued that, irrespective of the types of proteins, the increase in the rate of protein synthesis in the liver stimulated by GH is regulated at the cytoplasmic level. GH treatment of Snell dwarfs (also deficient in GH/IGF-I signaling) is associated with an increase in liver growth [74] and rate of protein synthesis [75]. Similar to the reduction of polysomes in long-lived yeast [76] and flies [55], comparisons of polysome profiles in dwarf and normal-size mice also showed a lower proportion of polysomes to monosomes, which are restored to normal with GH, but not with T3, treatment [77].…”

Hormonal status, creatine kinase and soccer: a need for research

“…CK delta = 1789.7 -33.1 x (f-testosterone) -482.3 x (fT 4 ) This model indicates that the lower the basal f-testosterone and fT 4 levels in the athletes, the greater the degree of CK elevation in response to the soccer match. This finding suggests that these athletes were experiencing greater degree of muscle damage during the match than those athletes with higher basal f-testosterone and fT 4 levels.…”

“…The anabolic actions of f-testosterone are well-established. But, fT 4 also has such anabolic actions by both direct and indirect means; that is, via the conversion of T 4 to T 3 and this hormone's subsequent anabolic effects (4,5). Interestingly, the latter hormone (fT 3 ) nearly reached significance to enter the regression model.…”

“…In the basal resting specimens this consisted of: total (t) T 3 , free (f) T 3 , tT 4 , fT 4 , TSH, t-testosterone, f-testosterone, growth hormone, insulin, cortisol, creatine kinase (CK), hematocrit, and hemoglobin. The post-match specimen measurements were: CK, hematocrit, and hemoglobin.…”