Effects of growth hormone and thyroxine on kidney insulin-like growth factor-I and renal growth in hypophysectomized rats

1993 ◽  
Vol 136 (3) ◽  
pp. 399-406 ◽  
Author(s):  
S. M. Marshall ◽  
A. Flyvbjerg ◽  
K. D. Jørgensen ◽  
J. Weeke ◽  
H. Ørskov
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Ratio ◽  
Treated Group ◽  
Body Weight Ratio ◽  
Kidney Weight ◽  
Renal Growth ◽  
Factor I ◽  
Igf I ◽  
Hypophysectomized Rats

ABSTRACT The effects of treatment for 11 days with human growth hormone (hGH; 140 μg/day), thyroxine (T4; 3 μg/day) and hGH + T4 on renal growth and content of insulin-like growth factor-I (IGF-I) in hypophysectomized rats have been compared with saline-treated hypophysectomized animals and intact control animals. Right kidney weight and kidney weight/body weight ratio remained low in the saline-treated group (313±9 vs 694±28 mg in controls on day 11, P<0·001 and 3·4±0·12 × 10−3 vs 4·2±0·10× 10−3, P< 0·005 respectively). In T4- and hGH-treated animals, kidney weight gain was similar (to 420 ± 14 and 450±22 mg on day 11 respectively, P>0·05), whilst the increase was greater in the group given hGH + T4 (to 572 ±34 mg, P< 0·001 compared with hGH- and T4-treated groups). The kidney weight/body weight ratio became normal in the T4- and hGH + T4-treated animals but remained low in the hGH-treated group. The renal content of IGF-I was low in the salinetreated animals throughout the study (92±10 ng/g on day 11 vs 219±8 ng/g in control animals, P< 0·001), but increased to a maximum of 88% above baseline on day 1 in the group given T4. In the hGH-and hGH + T4-treated groups, renal IGF-I concentration rose to a peak of 317% above baseline on days 2 to 4, then fell to the values seen in control animals on day 11 (hGH: 242±18 ng/g; hGH + T4: 320 ± 41 ng/g; controls: 219 ± 8 ng/g; P> 0·05 for all comparisons). Thus treatment with hGH or T4 results in similar kidney weight gain, despite a greater rise in the renal concentration of IGF-I in the hGH-treated animals. Treatment with both hGH + T4 leads to an increase in the renal concentration of IGF-I similar to that seen with hGH treatment alone, but a larger increase in kidney weight, suggesting that T4 does not stimulate renal growth via the IGF-I pathway and that growth promotion by hGH and T4 is additive. Journal of Endocrinology (1993) 136, 399–406

Kidney Weight and Recipient Body Weight Ratio Predict Long-Term Graft Outcome.

2014 ◽  
Vol 98 ◽  
pp. 612-613
Author(s):  
A. Akdur ◽  
M. Kirnap ◽  
E. Kolsarici ◽  
S. Yildirim ◽  
G. Moray ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Ratio ◽  
Body Weight Ratio ◽  
Kidney Weight ◽  
Graft Outcome

Stimulation of Renal Organic Base Transport by Uranyl Nitrate

1972 ◽  
Vol 50 (6) ◽  
pp. 533-538 ◽  
Author(s):  
G. H. Hirsch
Keyword(s):  
Body Weight ◽  
Uranyl Nitrate ◽  
Weight Ratio ◽  
Male Rats ◽  
Organic Base ◽  
Body Weight Ratio ◽  
Kidney Weight ◽  
Nitrate Treatment ◽  
Cortical Slices ◽  
Stimulation Of

Administration of 6 mg/kg uranyl nitrate to adult male rats resulted in a significant enhancement of N-methylnicotinamide (NMN) uptake by renal cortical slices when measured 24 or 48 h after injection. The accumulation of another organic base, tetraethylammonium (TEA), by renal cortical slices was also significantly increased by uranyl nitrate treatment, but transport of the organic acid p-aminohippurate (PAH) was not altered in these experiments. The kidney weight to body weight ratio was increased in treated rats. Accumulation of NMN by renal cortical slices was significantly enhanced within 8 h after administration of 6 mg/kg uranyl nitrate. NMN uptake was also significantly enhanced 24 and 48 h after administration of 0.5 or 1.0 mg/kg uranyl nitrate to rats. The nephrotoxicity produced by uranyl nitrate was not directly related to its induction of organic base transport. The data support the hypothesis that the organic base transport system can be selectively induced by appropriate stimuli. Treatment of rats with potassium chloride did not enhance NMN uptake by renal cortical slices.

Kidney IGF-I and renal hypertrophy in GH-deficient diabetic dwarf rats

1992 ◽  
Vol 262 (6) ◽  
pp. E956-E962 ◽  
Author(s):  
A. Flyvbjerg ◽  
J. Frystyk ◽  
R. Osterby ◽  
H. Orskov
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Insulin Like Growth Factor ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Glomerular Volume ◽  
Factor I ◽  
Igf I

Insulin-like growth factor I (IGF-I) has been proposed as a renotropic factor in initial diabetic kidney growth. To examine the effects of an isolated growth hormone (GH) and IGF-I deficiency on diabetic renal hypertrophy, dwarf rats were made diabetic and studied over a period of 7 days. Diabetic dwarf rats treated with human GH (hGH) or insulin and diabetic rats with intact pituitary were used as controls. In diabetic control animals kidney weight had increased by day 2 (P less than 0.01), and the increase amounted to 27% after 7 days, whereas untreated diabetic dwarf rats had a slower and lesser degree of kidney weight increase, reaching significance on day 7 only, amounting to 8%. hGH administration in diabetic dwarf rats increased the kidney weight on day 7 when compared with untreated diabetic dwarf rats (P less than 0.05) and was 19% over that of insulin-treated diabetic dwarf rats. The glomerular volume had increased by 43% in untreated diabetic control rats at day 7, compared with a 29% increase in untreated diabetic dwarf rats (P less than 0.05). hGH administration in diabetic dwarf rats increased the glomerular volume by 46%, comparable to the increase seen in diabetic control animals. Kidney IGF-I was increased on day 2 by 51 and 46% in saline- and hGH-injected diabetic dwarf rats, respectively, but a significantly higher increase in kidney IGF-I amounting to 96% was seen in diabetic control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The growth hormone-insulin-like growth factor I axis and renal glomerular function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1417-1422 ◽  
Author(s):  
R Hirschberg ◽  
J D Kopple
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Plasma Flow ◽  
Kidney Weight ◽  
Glomerular Function ◽  
Factor I ◽  
Igf I ◽  
Arteriolar Resistance ◽  
Single Nephron ◽  
Glomerular Ultrafiltration

This study examined whether maneuvers that chronically raise or lower serum insulin-like growth factor I (IGF-I), within physiological and pathophysiological ranges, will affect glomerular hemodynamics. Pair-fed Munich Wistar rats received, for 6 to 7 days, continuous s.c. infusions of human recombinant IGF-I (rhIGF-I; 125 micrograms/day), vehicle, or s.c. injection of a synthetic growth hormone-releasing hormone antagonist (GHRH-ANT) (N = 7 in each group). Infusion of rhIGF-I raised serum IGF-I to about 180% of control values, and GHRH-ANT injections lowered serum IGF-I to about 33% of control. The IGF-I infusion induced an increase in left kidney weight when expressed in absolute units but not when expressed as a percentage of body weight; there was also an increase in glomerular volume in the IGF-I treated rats. GFR, single nephron GFR, and single nephron plasma flow also rose with IGF-I infusion, and these changes were associated with decreased afferent and efferent arteriolar resistance and increased glomerular ultrafiltration coefficient. GHRH-ANT injection did not affect kidney weight or glomerular volume; however, GFR, single nephron GFR, and single nephron plasma flow were reduced in association with an increase in efferent arteriolar resistance. There also was a tendency, not significant, for the glomerular ultrafiltration coefficient to decrease. The findings that a low dose of rhIGF-I, which raised the serum IGF-I only modestly, increased glomerular ultrafiltration and that reducing serum IGF-I below control values decreased glomerular dynamics suggest that physiological or pathophysiological changes in IGF-I may affect and possible help to regulate glomerular function.(ABSTRACT TRUNCATED AT 250 WORDS)

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