Zinc (Zn) is an essential trace element that functions in cellular signaling. The mammalian target of rapamycin (mTOR) regulates the initiation of protein synthesis. The objective of this study was to determine whether Zn could stimulate protein phosphorylation in the mTOR pathway in vivo. Mice (C57BL/6J, n = 30) were fed Zn marginal diets (ZM, 5 mg/kg) for 4 weeks, followed by fasting (F) and/or refeeding with ZM or Zn supplemental (300 mg/kg, ZS) diets for 3 or 6 h. Plasma insulin was greater (P < 0.05) in refed animals as compared to F animals. Protein phosphorylation was detected using multiplex analysis and Western blotting. Multiplex analysis indicated greater (P < 0.05) p70 S6 kinase (p70S6K) and glycogen synthase kinase 3 (GSK-3 alpha/beta) phosphorylation in livers from 6-h refed ZS animals as compared to F animals. Western blots indicated increased (P < 0.05) Akt (Ser 473) phosphorylation in skeletal muscle from animals refed ZS diets for 3 and 6 h as compared to F animals. The ZS diet affected phosphorylation of GSK-3 (alpha/beta) in liver, as 3-h ZS refed animals had greater (P < 0.01) phosphorylation than F animals. These findings indicate that Zn may contribute to the initiation of protein synthesis as a signaling molecule in vivo.
Recent studies describe an association between poor iron status and obesity in humans, although the mechanism explaining this relationship is unclear. The present study aimed to determine the effect of moderate iron deficiency and physical activity (PA) on body composition in an animal model. Male Sprague-Dawley rats consumed iron-adequate (IA; 40 mg/kg) or moderately iron-deficient (ID; 9 mg/kg) diets ad libitum for 12 wk. Rats were assigned to 4 treatment groups (n = 10 per group): IA, sedentary (IAS); IA, PA (IAPA); ID, sedentary (IDS); or ID, PA (IDPA). Activity involved running on motorized running wheels at 4 m/min for 1 h/d for 5 d/wk. After 12 wk, ID rats were not anemic, but body iron stores were reduced as indicated by diminished (P < 0.05) femur iron compared with IA rats. Treatment group did not affect body weight or feed consumption. However, fat mass was greater (P < 0.05) in IDS rats (38.6 +/- 6.7%) than IAS (31.8 +/- 2.9%), IAPA (31.8 +/- 2.0%), and IDPA (32.8 +/- 4.5%) rats. Furthermore, lean body mass was diminished in IDS rats (58.7 +/- 6.8%) compared with IAS (65.6 +/- 3.0%), IAPA (65.6 +/- 2.1%), and IDPA (64.7 +/- 4.5%) rats. Thus, moderate iron deficiency may cause increased body fat accretion in rats and PA attenuates that effect.
Recent human studies demonstrate a relationship between iron deficiency and obesity, but it is not known whether physical training (PT) modulates the effects of iron deficiency on body composition and fat accretion. The objective of this study was to determine whether the effects of moderate iron deficiency on body fat accretion would be modulated by PT in growing rats. Male Sprague‐Dawley rats were fed iron adequate (IA, 45 mg/kg) or moderately iron deficient (ID, 10 mg/kg) diets ad libitum for 12 wks. Rats were assigned to four treatment groups (n = 10 per group): IA sedentary (IAS), IA physically trained (IAPT), ID sedentary (IDS), or ID physically trained (IDPT). PT involved running on motorized running wheels at 4 M/min for 1 h/d for 5 d/wk. After 12 wks, ID rats were not anemic, but iron status was diminished, as indicated by increased (P < 0.05) red cell distribution width ([mean ± SD] IAS = 13.8 ± 0.9, IAPT = 13.8 ± 1.1, IDS = 15.1 ± 0.5, IDPT = 14.1 ± 0.8 %). Body weight, lean body mass, and bone mineral content did not differ between groups. In contrast, the IDS rats had greater (P < 0.05) body fat as compared to all other groups (IAS = 31.8 ± 2.9, IAPT = 31.8 ± 2.0, IDS = 38.6 ± 6.7, IDPT = 32.8 ± 4.5 %). Thus, moderate iron deficiency may increase body fat accretion in growing animals, and PT appears to attenuate that effect. Research supported by MRMC.
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