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      Yeast hydrolysate induces longitudinal bone growth and growth hormone release in rats

      , , , ,
      Phytotherapy Research
      Wiley

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          The effects of treatment with recombinant human growth hormone on body composition and metabolism in adults with growth hormone deficiency.

          In a double-blind, placebo-controlled trial, we studied the effects of six months of growth hormone replacement in 24 adults with growth hormone deficiency. Most of the patients had acquired growth hormone deficiency during adulthood as a consequence of treatment for pituitary tumors, and all were receiving appropriate thyroid, adrenal, and gonadal hormone replacement. The daily dose of recombinant human growth hormone (rhGH) was 0.07 U per kilogram of body weight, given subcutaneously at bedtime. The mean (+/- SE) plasma concentration of insulin-like growth factor I increased from 0.41 +/- 0.05 to 1.53 +/- 0.16 U per liter during rhGH treatment. Treatment with rhGH had no effect on body weight. The mean lean body mass, however, increased by 5.5 +/- 1.1 kg (P less than 0.0001), and the fat mass decreased by 5.7 +/- 0.9 kg (P less than 0.0001) in the group treated with growth hormone; neither changed significantly in the placebo group. The basal metabolic rate, measured at base line and after one and six months of rhGH administration, increased significantly; the respective values were 32.4 +/- 1.4, 37.2 +/- 2.2, and 34.4 +/- 1.6 kcal per kilogram of lean body mass per day (P less than 0.001 for both comparisons). Fasting plasma cholesterol levels were lower (P less than 0.05) in the rhGH-treated group than in the placebo group, whereas plasma triglyceride values were similar in the two groups throughout the study. We conclude that growth hormone has a role in the regulation of body composition in adults, probably through its anabolic and lipolytic actions.
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            Premature mortality due to cardiovascular disease in hypopituitarism

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              Insulin-like growth factor 1 (IGF-1): a growth hormone.

              Z Laron (2001)
              To contribute to the debate about whether growth hormone (GH) and insulin-like growth factor 1 (IGF-1) act independently on the growth process. To describe growth in human and animal models of isolated IGF-1 deficiency (IGHD), such as in Laron syndrome (LS; primary IGF-1 deficiency and GH resistance) and IGF-1 gene or GH receptor gene knockout (KO) mice. Since the description of LS in 1966, 51 patients were followed, many since infancy. Newborns with LS are shorter (42-47 cm) than healthy babies (49-52 cm), suggesting that IGF-1 has some influence on intrauterine growth. Newborn mice with IGF-1 gene KO are 30% smaller. The postnatal growth rate of patients with LS is very slow, the distance from the lowest normal centile increasing progressively. If untreated, the final height is 100-136 cm for female and 109-138 cm for male patients. They have acromicia, organomicria including the brain, heart, gonads, genitalia, and retardation of skeletal maturation. The availability of biosynthetic IGF-1 since 1988 has enabled it to be administered to children with LS. It accelerated linear growth rates to 8-9 cm in the first year of treatment, compared with 10-12 cm/year during GH treatment of IGHD. The growth rate in following years was 5-6.5 cm/year. IGF-1 is an important growth hormone, mediating the protein anabolic and linear growth promoting effect of pituitary GH. It has a GH independent growth stimulating effect, which with respect to cartilage cells is possibly optimised by the synergistic action with GH.
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                Author and article information

                Journal
                PTR
                Phytotherapy Research
                Phytother. Res.
                Wiley
                0951418X
                10991573
                May 2009
                May 2009
                : 23
                : 5
                : 731-736
                Article
                10.1002/ptr.2720
                19107743
                cbe36f9c-3b64-4e15-a80f-b85cd02db2ea
                © 2009

                http://doi.wiley.com/10.1002/tdm_license_1.1

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