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)

Kidney tissue insulin-like growth factor I and initial renal growth in diabetic rats: Relation to severity of diabetes

1990 ◽  
Vol 122 (3) ◽  
pp. 374-378 ◽  
Author(s):  
Allan Flyvbjerg ◽  
Hans Ørskov
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Factor I ◽  
Urinary Glucose ◽  
Igf I ◽  
Growth Factor I

Abstract The initial renal hypertrophy in experimental diabetes is dependent on the prevailing blood glucose level and is associated with renal accumulation of insulinlike growth factor I. To investigate the relationship of blood glucose to kidney IGF-I, a graded range of diabetic aberration was established in young rats by iv injection of increasing amounts of streptozotocin (25–80 mg/kg) at day 0. In 30 diabetic rats the mean of day 1 and day 2 blood glucose concentrations ranged from 6.2 to 32.0 mmol/l and 24-h urinary glucose excretion (24–48 h) from 0.04 to 43.3 mmol/24 h. The right kidneys were removed after 48 h, weighed and their IGF-I concentration analysed by radioimmunoassay. Kidney IGF-I was positively correlated to blood glucose (r = 0.66, p<0.0001) as well as to 24-h urinary glucose output (r = 0.54, p<0.005). At this early stage, kidney weight already correlated to blood glucose (r = 0.60, p<0.0005). No relationship between kidney IGF-I and kidney weight was found. However, if animals with severe diabetes were excluded, a significant correlation could be established (r = 0.51, p = 0.01, N = 24). The results support the hypothesis that IGF-I plays a causal role in the initial renal hypertrophy of experimental diabetes.

Dual regulation of insulin-like growth factor I expression during renal hypertrophy

1989 ◽  
Vol 257 (2) ◽  
pp. F252-F261 ◽  
Author(s):  
R. Lajara ◽  
P. Rotwein ◽  
J. D. Bortz ◽  
V. A. Hansen ◽  
J. L. Sadow ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Compensatory Hypertrophy ◽  
Insulin Like Growth Factor ◽  
Renal Hypertrophy ◽  
Factor I ◽  
Collecting Ducts ◽  
Igf I ◽  
Hypophysectomized Rats ◽  
Growth Factor I

We examined the regulation of insulin-like growth factor I (IGF-I) in kidney during the renal hypertrophy produced by two different experimental models: growth hormone treatment of hypophysectomized rats and compensatory hypertrophy subsequent to unilateral nephrectomy. Immunostaining for IGF-I in collecting ducts was enhanced in kidneys from growth hormone-repleted hypophysectomized rats, and the levels of IGF-I mRNAs were increased. In compensatory hypertrophy, no enhancement of the intensity of immunostaining was observed in kidneys of nephrectomized rats until 5 days postnephrectomy, at which time immunostainable IGF-I was increased markedly in medullary collecting ducts of hypertrophied kidneys compared with kidneys from sham-operated animals. No difference in steady-state levels of any IGF-I mRNA species was detected in whole kidneys or in collecting ducts from nephrectomized or sham-operated rats at any time postnephrectomy. Our findings demonstrate an increase in both IGF-I mRNA and in immunostainable IGF-I in collecting duct in the setting of growth hormone-induced renal hypertrophy but suggest that other, possibly translational, mechanisms underlie the induction of IGF-I synthesis during compensatory hypertrophy.

Effects of refeeding of undernourished and insulin treatment of diabetic neonatal rats on IGF and IGFBP

1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Growth Factor ◽  
Mrna Expression ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Insulin Like Growth Factor ◽  
Neonatal Rats ◽  
Igf I ◽  
Serum Gh

The effect of refeeding and insulin treatment of undernourished and diabetic neonatal rats, respectively, on the regulation of insulin-like growth factor (IGF) and insulin-like growth factor binding protein (IGFBP) was investigated. The changes in body weight, insulinemia, glycemia, serum IGF-I, and growth hormone (GH) as well as the increase of the 30-kDa IGFBP in undernourished and diabetic neonatal rats previously shown elsewhere were reversed by refeeding and insulin treatment, respectively. Also, changes in liver mRNA expression of IGF-I and-II and IGFBP-1 and -2 were restored in refed undernourished and IGF-I and IGFBP-1 levels recovered in insulin-treated diabetic rats. However, serum GH was still below normal after rehabilitation in both situations. Thus the present results support the idea of a GH-independent IGF/ IGFBP regulation mediated by a balance of insulin and nutrients as has already been suggested in previous neonatal studies.

Longitudinal bone growth in vitro: effects of insulin-like growth factor I and growth hormone

1991 ◽  
Vol 124 (5) ◽  
pp. 602-607 ◽  
Author(s):  
Ben A. A. Scheven ◽  
Nicola J. Hamilton
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Bone Growth ◽  
Long Bone ◽  
Long Bones ◽  
Insulin Like Growth Factor ◽  
Serum Free ◽  
Factor I ◽  
Igf I

Abstract. Longitudinal growth was studied using an in vitro model system of intact rat long bones. Metatarsal bones from 18- and 19-day-old rat fetuses, entirely (18 days) or mainly (19 days) composed of chondrocytes, showed a steady rate of growth and radiolabelled thymidine incorporation for at least 7 days in serum-free media. Addition of recombinant human insulin-like growth factor-I to the culture media resulted in a direct stimulation of the longitudinal growth. Recombinant human growth hormone was also able to stimulate bone growth, although this was generally accomplished after a time lag of more than 2 days. A monoclonal antibody to IGF-I abolished both the IGF-I and GH-stimulated growth. However, the antibody had no effect on the growth of the bone explants in control, serum-free medium. Unlike the fetal long bones, bones from 2-day-old neonatal rats were arrested in their growth after 1-2 days in vitro. The neonatal bones responded to IGF-I and GH in a similar fashion as the fetal bones. Thus in this study in vitro evidence of a direct effect of GH on long bone growth via stimulating local production of IGF by the growth plate chondrocytes is presented. Furthermore, endogenous growth factors, others than IGFs, appear to play a crucial role in the regulation of fetal long bone growth.

scholarly journals Insulin-like growth factor-I, but not growth hormone, is dependent on a high protein intake to increase nitrogen balance in the rat

1999 ◽  
Vol 81 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Myriam Sanchez-Gomez ◽  
Kjell Malmlöf ◽  
Wilson Mejia ◽  
Antonio Bermudez ◽  
Maria Teresa Ochoa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Dietary Protein ◽  
Protein Diet ◽  
N Balance ◽  
Low Protein Diet ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Low Protein ◽  
Igf I

The aim of the present study was to investigate the influence of dietary protein level on the protein anabolic effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I). Female growing rats were fed on either a high- or a low-protein diet with crude protein contents of 222 and 83 g/kg respectively. The diets contained the same amount of metabolizable energy (15·1 MJ/kg) and were given during a 14 d period. During the same time, three groups of rats (n 8) on each diet received subcutaneous infusions of either saline, recombinant human GH (rhGH) or recombinant human IGF-I (rhIGF-I). rhGH and rhIGF-I were given in doses of 360 and 500 μg/d respectively. The low-protein diet alone reduced significantly (P < 0·05) IGF-I concentrations in serum and in tissue taken from the gastrocnemius muscle as well as IGF-I mRNA from the same muscle. The responses to rhGH and rhIGF-I in terms of muscle IGF-I and its mRNA were variable. However, when rhIGF-I was infused into rats on the high-protein diet, significantly elevated levels of IGF-I in muscle tissues could be observed. This was associated with a significantly (P < 0·05) increased N balance, whereas rhGH significantly (P < 0·05) enhanced the N balance in rats on the low-protein diet. Thus, it can be concluded that the level of dietary protein ingested regulates not only the effect of IGF-I on whole-body N economy but also the regulation of IGF-I gene expression in muscles. The exact mechanism by which GH exerts its protein anabolic effect, however, remains to be elucidated.

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