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Biomedical subjects

A Flyvbjerg

Publications and source records attributed to A Flyvbjerg.

At least 199 records · Page 11Linked to original sources
PubMed1991

Renal insulin-like growth factor I and growth hormone receptor binding in experimental diabetes and after unilateral nephrectomy in the rat.

We have measured specific binding of insulin-like growth factor I and growth hormone to renal plasma membranes from control, streptozotocin-diabetic, insulin-treated diabetic, uninephrectomised and combined diabetic-uninephrectomised male Wistar rats. Control, insulin-treated and uninephrectomised rats had similar body weights after 7 days (243 +/- 2 g), whereas diabetic and diabetic-uninephrectomised animals were significantly lighter (219 +/- 4 and 203 +/- 4 g, p less than 0.05). Blood glucose concentrations were similar in the diabetic and diabetic-uninephrectomised animals (around 26 mmol/l) but significantly lower in the insulin-treated group. Right kidney weight increased by 14% in the control, insulin-treated and sham-nephrectomised animals, by 33% in the diabetic group, 38% in thenephrectomised animals and 60% in the diabetic-nephrectomised group. The renal content of insulin-like growth factor I was similar and stable in the control, insulin-treated and sham-nephrectomised animals (208 +/- 14 ng/g wet weight) but rose to a peak of 669 +/- 35 ng/g in the diabetic group (p less than 0.001), 871 +/- 34 ng/g in the nephrectomised animals (p less than 0.001) and 1012 +/- 43 ng/g in the diabetic-uninephrectomised group (p less than 0.001). Maximum binding of insulin-like growth factor I fell on day 1 in the diabetic group (8.3 +/- 1.4 vs 5.2 +/- 0.71 x 10(-11) mol/l; p less than 0.01) but thereafter was identical to control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of insulin-like growth factor I infusion on renal hypertrophy in experimental diabetes mellitus in rats.

Initial diabetic renal hypertrophy is preceded by a transient increase in kidney insulin-like growth factor I suggesting that insulin-like growth factor I may be implicated in diabetic kidney growth. The present study was undertaken to examine the effects of exogenous insulin-like growth factor I infusion on diabetic renal hypertrophy at a time when renal insulin-like growth factor I concentration had returned to normal and the initial steep kidney growth rate had diminished to a much slower rate. Groups of rats with diabetes duration of 5 days were infused s.c. for 4 subsequent days with equimolar concentrations of insulin-like growth factor I (36 nmol/day) or insulin (35 nmol/day). Insulin infusion lowered blood glucose to a normal level within 2 days and induced an average body-weight gain of 9.3 +/- 0.6 g/day. Insulin-like growth factor I infused diabetic rats maintained the original diabetic state with blood glucose levels comparable to those of 0.154 mol/l NaCl-infused diabetic rats, but had nevertheless an average body-weight gain of 6.8 +/- 1.0 g/day while untreated diabetic rats had a lower body-weight gain amounting to 3.3 +/- 0.8 g/day (p less than 0.01). The kidney weight at day 9 in untreated diabetic animals was about 25% greater than that of non-diabetic control animals, while in insulin-like growth factor I treated diabetic rats a further increase (p less than 0.05) was seen, amounting to 36% above control level. No increase was seen in the insulin-treated diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Evidence that potassium deficiency induces growth retardation through reduced circulating levels of growth hormone and insulin-like growth factor I.

Growth retardation and impaired protein synthesis are major characteristics of potassium (K)-deficiency in animals and man. We have evaluated the effect of K-deficiency on growth, serum growth hormone (s-GH), insulin-like growth factor I (s-IGF-I), and insulin (s-insulin) in young rats. After 10 days on K-deficient fodder, 4 1/2-week-old rats showed a 54% reduction in serum potassium (s-K) and a weight gain that was reduced by 97%, compared with pair-fed controls. In addition, tail length, tibia length, and muscle weight of soleus in K-depleted animals were all significantly reduced compared with pair-fed controls. The growth retardation was accompanied by a 46% reduction in s-IGF-I, while s-insulin showed no decrease. K-repletion in animals depleted for 7 days showed complete normalization of s-K within 24 hours, in addition to a significant increase in both s-IGF-I and weight. In 4-week-old rats maintained on K-deficient fodder with variable K-content (1 to 260 mmol/kg) for 1 week, a strong correlation between the K-content of fodder and s-IGF-I could be established (r = .88, P less than .001), as well as between s-IGF-I and weight gain (r = .90, P less than .001). Furthermore, a stepwise reduction in basal s-GH was seen with the graded reduction of dietary K-content.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Role of insulin-like growth factor-1 and growth hormone in growth inhibition induced by magnesium and zinc deficiencies.

Nutritional deficiencies of magnesium or zinc lead to a progressive and often marked growth retardation. We have evaluated the effect of Mg and Zn deficiency on growth, serum insulin-like growth factor-1 (s-IGF-1), growth hormone (s-GH) and insulin (s-insulin) in young rats. In 3-week-old rats maintained on Mg-deficient fodder for 12 d the weight gain was reduced by about 34%, compared with pair-fed controls. This was accompanied by a 44% reduction in s-IGF-1, while s-insulin showed no decrease. After 3 weeks on Mg-deficient fodder, growth had ceased while serum Mg (s-Mg) and s-IGF-1 were reduced by 76 and 60% respectively. Following repletion with Mg, s-Mg was completely normalized in 1 week, and s-IGF-1 reached control level after 2 weeks. Growth rate increased, but the rats had failed to catch up fully in weight after 3.5 weeks. Absolute and relative pair-feeding were compared during a Mg repletion experiment. Absolute pair-fed animals were given the same absolute amount of fodder as the Mg-deficient rats had consumed the day before. Relative pair-fed animals were given the same amount of fodder, on a body-weight basis, consumed in the Mg-deficient group the day before. In a repletion experiment the two methods did not differ significantly from each other with respect to body-weight, muscle weight, tibia length and s-IGF-1, although there was a tendency towards higher levels in the relative pair-fed group. The peak in s-GH after growth hormone-releasing factor 40 (GRF 40) was 336 (SE 63) micrograms/l in 5-week-old rats that had been Mg depleted for 14 d, whereas age-matched control animals showed a peak of 363 (SE 54) micrograms/l (not significant). In 3-week-old rats maintained on Zn-deficient fodder for 14 d weight gain was reduced by 83% compared with pair-fed controls. Serum Zn (s-Zn) and s-IGF-1 were reduced by 80 and 69% respectively, while s-insulin was reduced by 66%. The Zn-deficient animals showed a more pronounced growth inhibition than that seen during Mg deficiency and after 17 d on Zn-deficient fodder s-IGF-1 was reduced by 83%. Following repletion with Zn, s-Zn was normalized and s-IGF-1 had increased by 194% (P less than 0.05) after 3 d. s-IGF-1, however, was not normalized until after 2.5 weeks of repletion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Inhibitory effect of octreotide on growth hormone-induced IGF-I generation and organ growth in hypophysectomized rats.

We investigated the effect of a somatostatin analogue octreotide (SMS) on the stimulatory effect of recombinant human growth hormone (hGH) on insulin-like growth factor I (IGF-I) generation and growth in hypophysectomized rats. Two weeks after hypophysectomy, treatment was given for 11 days with either saline, SMS (100 micrograms/day), hGH (140 micrograms/day), or hGH plus SMS. Compared with saline-injected controls, hGH stimulated body weight gain [1.1 +/- 0.7 vs. 40.9 +/- 0.8 (SE) g, P less than 0.001] and width of epiphysial cartilage (138.0 +/- 4.5 vs. 356 +/- 3.8 microns, P less than 0.001). Combined treatment with hGH and SMS significantly reduced both body weight gain (29.1 +/- 2.5 g, P less than 0.001) and width of epiphysial cartilage (315.3 +/- 5.8 microns, P less than 0.001) compared with the effects of hGH alone. During 11 days of hGH treatment, serum IGF-I increased from 22 +/- 5 to 1,288 +/- 92 micrograms/l (P less than 0.001) but increased only 40% (513 +/- 71 vs. 1,288 +/- 92 micrograms/l, P less than 0.001) when SMS was given in combination with hGH. In gastrocnemius muscle, heart, and lung, but not in liver, kidney, and brain, SMS suppressed organ weight increase when given both with and without hGH substitution. Thymus and gastrointestinal tract weight were significantly reduced in the group receiving SMS alone and tended to be reduced in the hGH-substituted group given SMS as well. Tissue IGF-I was increased in liver, lung, kidney, and heart with hGH treatment (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Insulin-like growth factor 1 and renal growth following ureteral obstruction in the rat.

The role of insulin-like growth factor 1 (IGF-1) in renal growth of obstructed and contralateral kidneys was investigated for 10 days following unilateral ureteric obstruction in male Wistar rats. The weight of the obstructed kidney increased rapidly, rising from 671 +/- 10 to 1,378 +/- 42 mg on day 10, an increase of 105%. IGF-1 content of the obstructed kidney was significantly less than in control kidneys from day 2 onwards, reaching a nadir of 70 ng/mg, a fall of 64%. The protein concentration, expressed as milligrams per gram kidney weight, also fell rapidly from 141 +/- 11 to 88 +/- 3 mg/g on day 6. The weight of the contralateral kidney increased by 32%, from 671 +/- 10 to 887 +/- 48 mg on day 10. The IGF-1 content of this kidney was increased by 48% from baseline on day 1 (268 +/- 23 vs. 191 +/- 13 ng/g) and remained increased compared to sham-operated animals on days 6 and 8. The protein content, expressed as milligrams per gram kidney weight, remained constant throughout the study. We conclude that in the acutely obstructed left kidney increasing kidney weight is associated with falling concentration of IGF-1 and protein and may be due to oedematous and reactive change. Growth of the contralateral kidney is preceded by a rise in the concentration of IGF-1 and may represent true renal compensatory growth.

Animals↗
PubMed1991

The influence of growth hormone and thyroxine on iodothyronine deiodinase activity in the liver, kidney and brown adipose tissue in hypophysectomized rats.

The effects of GH and T4 substitution on peripheral iodothyronine deiodinase activity in the liver, kidney and brown adipose tissue of hypophysectomized rats were investigated. Animals were treated with GH (140 micrograms hGH/day), T4 (3 micrograms/day), GH plus T4 (same doses), or saline. Rats were killed 0, 4, 7 or 11 days after treatment was started. Non-hypophysectomized, age-matched rats were killed after 0 and 11 days and served as controls. GH plus T4 restored body weight gain to normal, whereas GH alone and T4 alone did not. Tissue deiodinase activity and T3 concentrations were severely depressed in the hypophysectomized rats compared with non-hypophysectomized controls (to less than 10%). GH substitution in hypophysectomized rats led to a slight but significant elevation in tissue iodothyronine deiodinase activity in the liver and kidney, without concomitant increases in T3. Deiodinase activity in brown adipose tissue did not differ from that in saline-treated controls. T4 administration normalized deiodinase activity and tissue T3 content in all the evaluated tissues. GH plus T4 resulted in a lesser increase in deiodinase activity than T4 alone in the liver and kidney (p less than 0.01 at day 11), whereas no significant difference was observed in brown adipose tissue. In conclusion, GH stimulates iodothyronine deiodinase activity of the liver and kidney in hypophysectomized rats. Moreover, when GH is administered together with T4, the T4-stimulated enzyme activity in the liver and kidney is downregulated, suggesting that GH attenuates (or modulates) the T4 effect on this specific enzyme activity.

Adipose Tissue, Brown↗
PubMed1990

A short course of recombinant human growth hormone treatment stimulates osteoblasts and activates bone remodeling in normal human volunteers.

The effects of recombinant human growth hormone (rhGH) on biochemical markers of bone turnover and bone mineral content (BMC) were investigated in 20 normal male volunteers (aged 22-31 years) randomized to treatment for 7 days with either rhGH (0.1 IU/kg subcutaneously twice a day) or placebo. Serum somatomedin C rose during treatment (p less than 0.001) but was not significantly different from baseline at day 14. The fasting urinary hydroxyproline/creatinine (p less than 0.001) and calcium/creatinine ratios (p less than 0.01) increased during treatment and remained elevated for 4 and 2 weeks, respectively. Serum bone gamma-carboxyglutamic acid-containing protein (BGP) increased during treatment (p less than 0.001) and remained elevated for 6 months (p less than 0.02). Serum bone alkaline phosphatase (B-AP), after an initial fall in the treatment period (p less than 0.001), increased slightly in the following months (p less than 0.01). In the rhGH group BMC was significantly higher than the prestudy value at day 14 (p less than 0.05) but was unaltered at the end of study. The simultaneous increase in markers of bone resorption and formation during rhGH treatment followed by a decline in resorption parameters within a few weeks and the prolonged effect on BGP and B-AP demonstrate that rhGH treatment stimulates osteoblasts and activates bone remodeling.

Absorptiometry, Photon↗
PubMed1990

Kidney IGF-I mRNA in initial renal hypertrophy in experimental diabetes in rats.

It has recently been demonstrated that immunoassayable kidney insulin-like growth factor I concentration increases 24-48 h after induction of diabetes, preceding the initial renal hypertrophy. To elucidate whether this increase is due to increased local production we studied rat kidney insulin-like growth factor I gene expression during the first four days after induction of streptozotocin diabetes. Eighteen hours after injection with streptozotocin the diabetic animals were divided into two groups, one of which was treated with insulin, and daily for four days animals from each group were taken out for investigation. After four days the wet kidney weight had increased from baseline by 20% (from 687 +/- 23 to 827 +/- 6 mg (mean +/- SEM), p less than 0.01) in the untreated diabetic group, while no significant increase occurred in the insulin-treated group (687 +/- 23 vs 732 +/- 21 mg, NS). Kidney insulin-like growth factor I increased rapidly from baseline, the rise amounting to 52% after 48 h (from 271 +/- 11 to 411 +/- 32 ng/g, p less than 0.01) with a decline to control level on day four in the untreated diabetic group. Kidney insulin-like growth factor I remained unchanged in the insulin-treated diabetic group. Insulin-like growth factor I mRNA was measured by solution-hybridization assay. No differences were found in kidney insulin-like growth factor I mRNA between the two diabetic groups over the study period, while in liver, insulin-like growth factor I mRNA tended to be lower on day four in diabetic rats when compared to insulin-treated rats (p = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Additive increase in kidney insulin-like growth factor I and initial renal enlargement in uninephrectomized-diabetic rats.

The initial renal hypertrophy in experimental diabetes and in response to uninephrectomy is associated with renal accumulation of insulin-like growth factor I (IGF-I). Since the combination of diabetes and nephrectomy almost doubles the initial renal growth rate the aim of the present study was to investigate the kidney IGF-I levels in the combined situation in uninephrectomized diabetic rats. Three experimental groups were exposed to either unilateral nephrectomy, streptozotocin-diabetes or both conditions and for four days animals from each group were taken out for investigation. After 4 days the wet kidney weight increased from baseline by 31% (from 661 +/- 16 mg (SEM) to 866 +/- 27 mg) (P less than 0.01) in the uninephrectomized group, 32% (to 872 +/- 18 mg) (P less than 0.01) in the diabetic group and 46% (to 962 +/- 27 mg) (P less than 0.01) in the uninephrectomized-diabetic group. Kidney IGF-I concentrations were analyzed by radioimmunoassay and the increase from baseline on day 2 was 74% (from 262 +/- 12 ng/g (SEM) to 456 +/- 21 ng/g) (P less than 0.01) in the uninephrectomized group, 58% (to 414 +/- 18 ng/g) (P less than 0.01) in the diabetic group and 176 +/- % (to 722 +/- 56 ng/g) (P less than 0.01) in the combined group. Thereafter a decline in kidney IGF-I occurred in all groups, being normal at day 4 for the diabetic group, but still significantly higher in the uninephrectomized and uninephrectomized-diabetic groups compared to controls (P less than 0.05%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Na(+)-K+ pump in rat muscle: effects of hypophysectomy, growth hormone, and thyroid hormone.

We investigated the effects of growth hormone and thyroid hormone on the synthesis of Na(+)-K+ pumps in rat soleus muscle. Hypophysectomized rats were treated for 11 days with saline, human growth hormone (hGH; 140 micrograms/day), thyroxine (T4; 3 micrograms/day), or hGH plus T4. Age-matched nonhypophysectomized control rats received no treatment. The concentration of Na(+)-K+ pumps was reduced by 75% in the hypophysectomized rats. Treatment with hGH alone or combined with T4 restored the growth rate, whereas T4 alone did not stimulate growth. In contrast, the synthesis of Na(+)-K+ pumps was only responsive to T4 treatment when given alone or in combination with hGH. The concentration of Na(+)-K+ pumps increased around threefold in the T4-treated groups and showed full normalization to the control level after 11 days of treatment. It is concluded that growth hormone does not play any major role in the de novo synthesis of Na(+)-K+ pumps in skeletal muscle. More important, thyroid hormone, also at physiological doses, seems to be the major endocrine factor determining the concentration of Na(+)-K+ pumps in skeletal muscle.

Animals↗
PubMed1990

Short-term effects of growth hormone on fuel oxidation and regional substrate metabolism in normal man.

Primarily by increasing the availability of lipid intermediates, GH is likely to have profound effects on substrate consumption rates. To examine the short term actions of GH on glucose turnover, fuel oxidation and regional forearm metabolism, six normal volunteers were each studied twice for 5.5 h after having received a 4-h infusion of GH (20 ng/kg.min) or saline. GH induced slightly falling plasma glucose levels, acute 40-50% decreases in forearm glucose uptake, and no change in glucose turnover. Furthermore, substantial increases in circulating concentrations and forearm uptake of nonesterified fatty acids and 3-hydroxybutyrate were recorded. Although GH infusion was followed by a 50% reduction of forearm alanine release hepatic nitrogen excretion seemed unaffected. Energy expenditure was not influenced by GH, but the non-protein respiratory exchange ratio decreased from a basal value of 0.778 +/- 0.008 to 0.732 +/- 0.007 after GH treatment (P less than 0.05). Correspondingly, lipid oxidation increased from 1.20 +/- 0.06 to 1.48 +/- 0.09 mg/kg.min, and glucose oxidation decreased from 0.97 +/- 0.12 to 0.39 +/- 0.06 mg/kg.min (P less than 0.05). Nonoxidative glucose utilization tended to increase. These data indicate that GH, by promoting lipid utilization and decreasing glucose oxidation, diminishes the need for gluconeogenesis and, therefore, could be protein preserving in the long term. Overall, we found no evidence of GH having acute insulin-like effects on glucose metabolism. GH appears to increase glucose storage, leaving total energy expenditure unaffected.

3-Hydroxybutyric Acid↗
PubMed1990

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

The initial renal hypertrophy in experimental diabetes is dependent on the prevailing blood glucose level and is associated with renal accumulation of insulin-like 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 less than 0.0001) as well as to 24-h urinary glucose output (r = 0.54, p less than 0.005). At this early stage, kidney weight already correlated to blood glucose (r = 0.60, p less than 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.

Animals↗
PubMed1990

Early changes in thyroid hormone metabolism in the heart, liver, and brown adipose tissue during the induction of low T3 syndrome in streptozotocin-diabetic rats.

In order to elucidate the day-by-day development of low T3 syndrome, we made rats diabetic by an injection of streptozotocin. Untreated controls killed at day 0 and rats treated for 8 days with insulin after they had received streptozotocin served as controls. Sub-groups of animals were killed 1, 2, 3, 4 and 8 days after streptozotocin. In serum, heart and liver, T3 was depressed to less than 50% of controls at day 4, whereas the insulin-treated rats differed from controls only as to heart T3. Heart iodothyronine 5'-deiodinase activity was depressed to a minimum at day 3 and depression was not prevented by insulin. Liver iodothyronine 5'-deiodinase activity had not reached a minimum at day 8, and again, insulin treatment did not normalize this parameter. T3 contents and iodothyronine 5'-deiodinase activity in brown adipose tissue did not differ from values in controls at any point of time. Thus, in the rats with low T3 syndrome induced by streptozotocin-diabetes, a lowered iodothyronine 5'-deiodinase activity is not fully inhibited by insulin treatment, whereas the T3 content in the liver is re-established during an observation period of 8 days. A direct toxic effect of streptozotocin seems unlikely as an in vitro study showed no influence of streptozotocin on iodothyronine 5'-deiodinase activity in the liver. The study thus indicates that iodothyronine 5'-deiodinase activity in the heart and liver is depressed in experimental diabetes, despite near optimal regulation of blood glucose, and we suggest that lowered intracellular T3 production could, after some time, result in a hypothyroid state in different tissues.

Adipose Tissue, Brown↗
PubMed1989

Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats.

In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. The kidney hypertrophy in untreated diabetic animals amounted to 23% four days after streptozotocin injection and followed an increase in kidney somatomedin C content of 60% reaching the maximum after 48 h. In young and old uninephrectomized rats kidney growth was 19% and 16% after four days. In young animals a prompt increase of 50% in kidney somatomedin C was seen as reaching the maximum after 24 h, while the somatomedin C content in kidneys from old animals was maximal after 48 h (increase of 58%) in good accordance with the slightly slower kidney growth. The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. It is noteworthy that Sandostatin administration did not alter the metabolic state in diabetic animals indicating that the inhibition of kidney hypertrophy could not be attributed to improved metabolic control. The results thus support the concept that somatomedin C is involved in initial diabetic and post-nephrectomy renal growth.

Aging↗
PubMed1989

The metabolic clearance rate, serum half-time and apparent distribution space of authentic biosynthetic human growth hormone in growth hormone-deficient patients.

We studied the metabolic clearance rate (MCR) serum half-time (t1/2) and apparent distribution space (DS) of unlabelled, authentic, biosynthetic human growth hormone (B-hGH) in 9 GH-deficient patients by means of the constant iv infusion to equilibrium technique. B-hGH was infused for 3 h at a rate of 33 ng.kg-1.min-1 after which the disappearance from serum of GH was followed for 1 h. The mean +/- SEM values for MCR, t1/2 and DS were: 2.3 +/- 0.6 ml.kg-1.min-1, 21.1 +/- 1.7 min and 67.6 +/- 14.6 ml/kg, respectively. The disappearance of GH was monoexponential for the first 30 min, during which 75% of the GH had been cleared. The disappearance rate during the last 30 min of the observation period was somewhat lower, still approximately 90% of the GH had been eliminated after 60 min.

Adolescent↗
PubMed1988

Kidney tissue somatomedin C and initial renal growth in diabetic and uninephrectomized rats.

Kidney growth after induction of experimental diabetes in rats was compared to compensatory renal growth in response to unilateral nephrectomy. After 4 days of diabetes, kidney weight had increased from 816 +/- 21 mg (SEM) to 940 +/- 42 mg (15%). In insulin-treated diabetic rats kidney weight was unchanged at the end of the study, namely 828 +/- 15 mg. In unilaterally nephrectomised rats kidney weight increased from 840 +/- 20 mg (SEM) to 1050 +/- 60 mg during 4 days (24%). We observed increased kidney content of somatomedin C in both diabetic and uninephrectomized rats. In untreated diabetic rats it was maximal after 48 h, with an increase of 77% (3469 +/- 312 ng/g (SEM) versus 1961 +/- 173 ng/g). After 4 days the somatomedin C content had returned to initial levels. In insulin-treated rats somatomedin C content did not increase during the observation period. The somatomedin C content of the remaining kidney after unilateral nephrectomy was maximal after 24 h with an increase of 58% (from 1340 +/- 203 ng/g (SEM) to 2122 +/- 214 ng/g). The somatomedin C content returned to normal at day 4. Serum somatomedin C declined insignificantly in diabetic animals during the experimental period, but a significant decrease (p less than 0.02) was found in uninephrectomized rats. This study demonstrates that kidney somatomedin C peaks during the first or second day after uninephrectomy or induction of diabetes, respectively, and that insulin treatment sufficient to prevent kidney growth abolishes the increase. These similar rapid initial hypertrophies/hyperplasies may thus be dependent on local somatomedin C formation.

Animals↗