scholarly journals Effects of Daidzein on Body Weight Gain, Serum IGF-I Level and Cellular Immune Function in Intact Male Piglets

2002 ◽  
Vol 15 (7) ◽  
pp. 1066-1070 ◽  
Author(s):  
Wang Genlin ◽  
Zhang Xiangying ◽  
Han Zhaoyu ◽  
Liu Zhaobin ◽  
Liu Weirong
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Immune Function ◽  
Body Weight Gain ◽  
Intact Male ◽  
Cellular Immune Function ◽  
Igf I ◽  
Cellular Immune

scholarly journals IGF-I and IGF-I-binding proteins in rats with adjuvant-induced arthritis given recombinant human growth hormone

2000 ◽  
Vol 165 (3) ◽  
pp. 537-544 ◽  
Author(s):  
I Ibanez De Caceres ◽  
MA Villanua ◽  
L Soto ◽  
AI Martin ◽  
A Lopez-Calderon
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Binding Proteins ◽  
Body Weight Gain ◽  
Recombinant Human Growth Hormone ◽  
Gh Treatment ◽  
Adjuvant Induced Arthritis ◽  
Igf I ◽  
Igfbp 3

Adjuvant-induced arthritis in rats is associated with growth failure, hypermetabolism and accelerated protein breakdown. We have previously reported that adjuvant-induced arthritis in rats results in a decrease in body weight gain, pituitary GH mRNA, circulating GH and IGF-I together with an increase in serum IGF-binding proteins (IGFBPs). The aim of this study was to analyze the role of GH in the decrease in body weight and in the alterations in the IGF-I system observed in chronic inflammation. Male Wistar rats were injected with complete Freund's adjuvant and 16 days later arthritic rats were injected daily with recombinant human GH (rhGH) (3 IU/kg s.c.) for 8 days; control rats received 250 microl saline. Arthritis significantly decreased body weight gain and serum IGF-I. These decreases were not due to the reduced food intake, since in pair-fed rats they were not observed. Furthermore, administration of rhGH to arthritic rats increased body weight gain without modifying food intake. To further investigate the effect of GH administration, 14 days after adjuvant injection both control and arthritic rats were treated with 0, 1.5, 3 or 6 IU/kg of rhGH. GH treatment at the dose of 3 and 6 IU/kg significantly increased body weight gain in arthritic rats. GH administration, at the higher dose of 6 IU/kg, increased hepatic and serum concentrations of IGF-I in both control and arthritic rats. In control rats, rhGH at the three doses assayed increased circulating IGFBP-3. GH treatment in arthritic rats decreased IGFBP-1 and -2, and did not modify IGFBP-4. GH treatment at the dose of 3 IU/kg also decreased circulating IGFBP-3 in arthritic rats. These data suggest that GH treatment can ameliorate the catabolism observed in adjuvant-induced arthritis, an effect mediated, at least in part, by modifications in the circulating IGFBPs.

Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone

1989 ◽  
Vol 122 (1) ◽  
pp. 79-86 ◽  
Author(s):  
D. J. Flint ◽  
M. J. Gardner
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Growth Factor ◽  
Body Weight Gain ◽  
Neonatal Rat ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Rat Growth ◽  
Growth Factor I

ABSTRACT Treatment of rats for 24 h on day 2, 10 or 20 of age with a specific antiserum to rGH (anti-(rGH)), GH, bromocriptine (CB-154) or prolactin failed to influence body weight gain or serum concentrations of insulin-like growth factor-I (IGF-I). On day 28 of age, however, anti-(rGH) completely inhibited body weight gain and markedly reduced circulating IGF-I concentrations, effects which were completely prevented by exogenous ovine GH (oGH). When administered to control rats on day 28 oGH caused supranormal weight gain and serum IGF-I concentrations. These results suggested that GH does not play a significant role in growth or regulation of serum IGF-I until after day 20 of age. By contrast, when anti-(rGH) was given for 4 consecutive days beginning on day 2 of life, body weight gain was reduced within 48 h and remained so until at least 28 days of age. Tail length was also significantly reduced. The effect was due to inhibition of GH effects since serum GH concentrations were low and exogenous GH prevented the effect. Inhibition of growth during the first 14 days of life occurred in the absence of any effect on serum IGF-I although by 21 days of age serum IGF-I was considerably lower than in control rats. The prolonged reduction in growth after treatment has stopped appeared to be due to a cytotoxic effect on the pituitary gland since pituitary weight and GH but not prolactin content were significantly decreased. The data are consistent with the hypothesis that in the neonate GH may be processed in serum so that a proportion of it is not recognized by an antiserum to pituitary GH. It would appear that inhibition of GH secretion reduces growth rate by at least 30–40% up to 14 days of age, 50% by 21 days of age and completely by 28 days. Effects of GH on growth could not be fully explained by regulation of serum IGF-I concentrations. Journal of Endocrinology (1989) 122, 79–86

Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation

2007 ◽  
Vol 292 (6) ◽  
pp. E1656-E1665 ◽  
Author(s):  
Miriam Granado ◽  
Ana I Martín ◽  
Mª Ángeles Villanúa ◽  
Asunción López-Calderón
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Weight Gain ◽  
Muscle Wasting ◽  
Body Weight Gain ◽  
Chronic Arthritis ◽  
Factor I ◽  
Tnf Α ◽  
Igf I ◽  
Cox 2

Chronic arthritis induces cachexia associated with an inhibition of the growth hormone (GH)-insulin-like growth factor-I (IGF-I) system and an activation of the E3 ubiquitin-ligating enzymes muscle atrophy F-box (MAFbx) and muscle Ring finger 1 (MuRF1) in the skeletal muscle. The aim of this work was to study the role of cyclooxygenase (COX)-2 in chronic arthritis-induced cachexia. Arthritis was induced in rats by Freund's adjuvant injection, and the effects of two COX inhibitors (indomethacin, a nonspecific inhibitor, and meloxicam, a selective COX-2 inhibitor on pituitary GH and on liver and serum IGF-I levels) were tested. Arthritis decreased body weight gain and GH and liver IGF-I gene expression. In the arthritic rats, both inhibitors, indomethacin and meloxicam, prevented the inhibitory effect of arthritis on body weight gain. Indomethacin and meloxicam administration to arthritic rats increased pituitary GH and liver IGF-I mRNA as well as serum levels of IGF-I. These data suggest that induction of COX-2 during chronic inflammation is involved in the inhibition of the GH-IGF-I axis and in the body weight loss. In the gastrocnemius muscle, arthritis increased the gene expression of tumor necrosis factor (TNF)-α, the E3 ubiquitin-ligating enzymes MAFbx and MuRF1, as well as of IGF-I and IGF-binding protein-5 (IGFBP-5). Inhibition of COX-2 by meloxicam administration increased gastrocnemius weight and decreased MAFbx, MuRF1, TNF-α, and IGFBP-5 gene expression. In summary, our data indicate that chronic arthritis-induced cachexia and muscle wasting are mediated by the COX-2 pathway resulting in a decreased GH-IGF-I secretion and increased expression of MAFbx and MuRF1 mRNA.

scholarly journals A GH receptor antisense oligonucleotide inhibits hepatic GH receptor expression, IGF-I production and body weight gain in normal mice

2006 ◽  
Vol 189 (1) ◽  
pp. 147-154 ◽  
Author(s):  
G Tachas ◽  
S Lofthouse ◽  
C J Wraight ◽  
B F Baker ◽  
N B Sioufi ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Antisense Oligonucleotide ◽  
Body Weight Gain ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Receptor Mrna ◽  
Gh Receptor ◽  
Igf I

Diabetic retinopathy and acromegaly are diseases associated with excess action of GH and its effector IGF-I, and there is a need for improved therapies. We have designed an optimised 2′-O-(2-methoxyethyl)-modified phosphorothioate oligodeoxynucleotide, ATL 227446, and demonstrated its ability to suppress GH receptor mRNA in vitro. Subcutaneous injections of ATL 227446 reduced GH receptor mRNA levels, GH binding activity and serum IGF-I levels in mice after seven days of dosing. The reduction in serum IGF-I could be sustained for over ten weeks of dosing at therapeutically relevant levels, during which there was also a significant decrease in body weight gain in antisense-treated mice relative to saline and mismatch control-treated mice. The findings indicate that administration of an antisense oligonucleotide to the GH receptor may be applicable to human diseases in which suppression of GH action provides therapeutic benefit.

Reduced serum concentrations of insulin-like growth factor-I (IGF-I) in protein-restricted growing rats are accompanied by reduced IGF-I mRNA levels in liver and skeletal muscle

1991 ◽  
Vol 130 (2) ◽  
pp. 305-312 ◽  
Author(s):  
M. J. VandeHaar ◽  
B. M. Moats-Staats ◽  
M. L. Davenport ◽  
J. L. Walker ◽  
J.-M. Ketelslegers ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Protein Restriction ◽  
Mrna Abundance ◽  
Factor I ◽  
Growing Rats ◽  
Low Protein ◽  
Igf I

ABSTRACT The serum concentration of insulin-like growth factor-I (IGF-I) is reduced in growing rats fed a low-protein diet, and this decrease is age-dependent, being more pronounced in younger animals. To determine whether this decrease in serum IGF-I is related to a decrease in IGF-I mRNA, growing female rats were given free access to either a 15% protein-sufficient or a 5% protein-deficient diet for 1 week. Protein restriction in 4-week-old rats decreased body weight gain by 44% (P < 0·001) compared with 4-week controls), serum IGF-I concentration by 67% (P < 0·001) and liver IGF-I mRNA abundance by 51% (P < 0·001). During week 6, protein restriction for 1 week resulted in a 20% increase in food intake with no change in weight gain, a 38% reduction in serum IGF-I (P < 0·001 compared with 6-week controls) and a 39% decrease in liver IGF-I mRNA (P < 0·001). The serum IGF-I concentration was highly correlated (r = 0·80; P < 0·001) with the hepatic IGF-I mRNA concentration. Skeletal muscle IGF-I mRNA abundance was also decreased significantly by protein restriction (37% at week 4, P<0·001, and 24% at week 6, P < 0·01) and was closely correlated (r = 0·71; P < 0·001) with body weight gain. Liver GH-binding protein and GH receptor mRNA abundance were reduced by 1 week of protein deprivation at week 6 but not at week 4. We conclude that the reduced serum IGF-I of young rats fed a low-protein diet is due, in part, to reduced liver IGF-I mRNA, and that these changes are not dependent on GH binding. Decreased skeletal muscle IGF-I mRNA during protein restriction is consistent with an autocrine/paracrine action of IGF-I in muscle. Journal of Endocrinology (1991) 130, 305–312

scholarly journals Relationship between serum concentrations of leptin, soluble leptin receptor, testosterone and IGF-I, and growth during the first year of postnatal life in the male rhesus monkey, Macaca mulatta

2005 ◽  
Vol 153 (1) ◽  
pp. 153-158 ◽  
Author(s):  
Ganapathy K Bhat ◽  
Tony M Plant ◽  
David R Mann
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Serum Testosterone ◽  
First Year ◽  
Postnatal Life ◽  
Study Objective ◽  
Serum Leptin ◽  
Igf I ◽  
Male Rhesus

Objectives: Subnormal leptin levels in low birth weight infants may allow for catch-up growth during infancy. Scant data are available that relate growth with circulating leptin during normal infancy in primates. The current study objective was to examine the association between serum leptin, its soluble receptor (sOB-R), testosterone and IGF-I concentrations, and body weight during infancy in male rhesus monkeys. Design: Hormone levels were assessed longitudinally in animals (n = 7) from birth until 1 year of age. Results: Body weight increased during the first 6 months of life and was strongly correlated with rising IGF-I levels and, as IGF-I plateaued and then declined during the second half of the year, body weight gain decelerated. In contrast, leptin levels declined gradually with age during the first year of life in conjunction with increasing body weight. There was no association between body weight gain and serum leptin levels or between serum testosterone and leptin values. Since sOB-R levels also declined with leptin values, it does not appear that levels of bioavailable leptin changed during infancy. Conclusions: The data do not support the contention that leptin regulates growth during infancy, but the close association between IGF-I levels and body weight suggested that this hormone may regulate growth in infant male monkeys. The failure to observe an association between serum testosterone and leptin concentrations suggested that leptin is not involved in the activation of the hypothalamic–pituitary –testicular axis during this developmental period.

Systemic IGF-I administration attenuates the inhibitory effect of chronic arthritis on gastrocnemius mass and decreases atrogin-1 and IGFBP-3

2010 ◽  
Vol 299 (2) ◽  
pp. R541-R551 ◽  
Author(s):  
María López-Menduiña ◽  
Ana Isabel Martín ◽  
Estíbaliz Castillero ◽  
María Angeles Villanúa ◽  
Asunción López-Calderón
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Weight Gain ◽  
Soleus Muscle ◽  
Body Weight Gain ◽  
Inhibitory Effect ◽  
Chronic Arthritis ◽  
Igf I ◽  
Igfbp 3

Adjuvant arthritis is an animal model of rheumatoid arthritis that decreases liver and circulating IGF-I as well as skeletal muscle mass. The aim of this work was to elucidate whether IGF-I administration was able to prevent the effect of arthritis on body weight and on two skeletal muscles, gastrocnemius and soleus. On day 4 after adjuvant injection, control and arthritic rats were treated with IGF-I (100 μg/kg sc) two times a day, until day 15 when all rats were killed. Arthritis decreased body weight gain and gastrocnemius weight. In arthritic rats, IGF-I treatment increased body weight gain and gastrocnemius weight, without modifying food intake or the external signs of arthritis. Arthritis increased atrogin-1 and muscle ring finger 1 (MuRF1) gene expression in the gastrocnemius and to a lesser extent in the soleus muscle. IGF-I attenuated the arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius, whereas it did not modify the expression of these genes in the soleus muscle. Arthritis also increased IGF-binding protein (IGBP)-3 and IGFBP-5 gene expression in gastrocnemius and soleus, whereas IGF-I administration decreased IGFBP-3, but not IGFBP-5, gene expression in both muscles. In both groups of arthritic rats and in control rats treated with IGF-I, proliferating cell nuclear antigen and myogenic differentiation proteins were increased in the gastrocnemius. These data suggest that the inhibitory effect of chronic arthritis on skeletal muscle is higher in fast glycolytic than in slow oxidative muscle and that IGF-I administration attenuates this effect and decreases atrogin-1 and IGFBP-3 gene expression.

Effects of constant infusion with insulin-like growth factor-I (IGF-I) to immature female rats on body weight gain, tissue growth, and sexual function

Endocrine ◽  
1997 ◽  
Vol 6 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Nadine M. Gruaz ◽  
Violaine d'Allèves ◽  
Yves Charnay ◽  
Anna Skotther ◽  
Sven Ekvärn ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Growth Factor ◽  
Body Weight Gain ◽  
Tissue Growth ◽  
Female Rats ◽  
Constant Infusion ◽  
Immature Female ◽  
Factor I ◽  
Igf I

Reduced liver insulin-like growth factor-I gene expression in young zinc-deprived rats is associated with a decrease in liver growth hormone (GH) receptors and serum GH-binding protein

1995 ◽  
Vol 144 (3) ◽  
pp. 449-456 ◽  
Author(s):  
N X Ninh ◽  
J-P Thissen ◽  
D Maiter ◽  
E Adam ◽  
N Mulumba ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Binding Protein ◽  
Normal Diet ◽  
Mrna Levels ◽  
Zinc Depletion ◽  
Igf I ◽  
Serum Gh ◽  
Gh Receptors

Abstract Zinc depletion attenuates growth and decreases circulating IGF-I. To investigate the mechanisms responsible for the IGF-I decline, we determined the effects of dietary zinc (Zn) deficiency on body and organ growth, serum IGF-I, serum GH-binding protein (GHBP), liver GH receptors and liver expression of their corresponding gene. After 1 week of adaptation to a normal zinc diet, a zinc-deficient diet (ZD; Zn, 0 p.p.m.) or a zinc-normal diet (CTR; Zn, 75 p.p.m.) was available ad libitum to 4-week-old Wistar rats for 4 weeks. Pair-fed animals (PF) received the zinc-normal diet in the same absolute amount as that consumed the day before by the ZD group. The food intake of ZD and PF rats was reduced by 32% (P<0·001) compared with the CTR group. Zinc depletion specifically reduced body weight gain (−22%, P<0·05), serum IGF-I concentrations (−52%, P<0·001), hepatic GH receptors (−28%; P<0·05) and serum GHBP levels (−51%; P<0·05), compared with the PF group. GH concentrations were reduced in ZD animals compared with CTR rats (P<0·01). The caloric restriction of PF animals also decreased body weight gain (−50%, P<0·001), serum IGF-I concentrations (−21%, P<0·05), liver GH receptors (−38%, P<0·001) and serum GHBP levels (−38%, P<0·01), when compared with the CTR group. Both ZD and PF groups had reduced liver IGF-I and GH receptor/GHBP mRNA levels in comparison with the CTR group (P<0·01). However, only liver IGF-I mRNA levels were specifically reduced by zinc deficiency (ZD vs PF rats; P<0·05). Our observations suggest that beside the decline of GH secretion, decreased hepatic GH receptors and/or GHBP concentrations might be responsible for the decline of circulating IGF-I in ZD animals. Journal of Endocrinology (1995) 144, 449–456

Effects of insulin-like growth factor-I peptides in rats with acute renal failure

1994 ◽  
Vol 140 (1) ◽  
pp. 23-32 ◽  
Author(s):  
A A Martin ◽  
C M Gillespie ◽  
L Moore ◽  
F J Ballard ◽  
L C Read
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Body Weight ◽  
Acute Renal Failure ◽  
Weight Gain ◽  
Growth Factor ◽  
Body Weight Gain ◽  
Factor I ◽  
Renal Ischaemia ◽  
Igf I

Abstract The effect of insulin-like growth factor-I (IGF-I) administration on body weight gain and the rate of recovery of renal function was investigated in rats following an acute episode of renal ischaemia. Since the des(1–3)IGF-I and LR3IGF-I variant forms of IGF-I have been shown to be more potent than IGF-I, their effects were also examined. Acute renal failure was produced in male Sprague–Dawley rats by clamping both renal arteries for 45 min. Treatment was commenced at the time of renal artery occlusion with vehicle (0·1 mol acetic acid/l; control group), IGF-I (2·0 mg/kg per day), des(1–3)IGF-I (2·0 mg/kg per day) or LR3IGF-I (1·5 mg/kg per day) by s.c. osmotic pump, and continued for 7 days, with rats being held in metabolism cages. Glomerular filtration rate (GFR) was estimated by the use of 51Cr-EDTA continuously infused i.p. via osmotic pump. Following the episode of renal ischaemia, body weight gain and nitrogen retention were significantly improved in all three peptide-treated groups, and serum urea concentrations were reduced in the groups treated with IGF-I and des(1–3)IGF-I. However, there was no evidence of the variants having any increased potency over the growth effects of IGF-I itself. GFR was significantly reduced, urine output was increased and urinary concentrating ability was reduced in all groups compared with normal rats, with no significant effect of the IGF peptides being apparent. A closer examination of the acute effects of LR3IGF-I on renal function was undertaken by measuring GFR for 3 days before and 3 days after renal ischaemia in two groups of rats, treated for the latter 3 days with either vehicle (controls) or LR3IGF-I (1·5 mg/kg per day). LR3IGF-I treatment following renal ischaemia resulted in a significantly greater fall in GFR than in controls, urinary osmolality was also significantly reduced, and fractional excretion of sodium was increased. In addition, there was histological evidence of a greater degree of tubular epithelial calcification in the kidneys of the rats treated with LR3IGF-I. This study showed that administration of IGF peptides at doses sufficient to cause significant improvement in anabolic status did not improve renal function in rats following an acute episode of renal ischaemia. Indeed the LR3IGF-I variant of IGF-I had a deleterious effect on renal function in the early stage of the recovery period. Journal of Endocrinology (1994) 140, 23–32

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