Biomedical subjects

H Orskov

Publications and source records attributed to H Orskov.

At least 163 records · Page 9Linked to original sources

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

Physiological levels of plasma non-esterified fatty acids impair forearm glucose uptake in normal man.

1. The purpose of the present study was to maintain physiological plasma non-esterified fatty acid levels and to (i) examine their effect on skeletal muscle insulin-stimulated glucose uptake and metabolite exchange using the forearm technique, and (ii) evaluate their effect on whole-body glucose uptake and fuel oxidation. 2. Intralipid (10%) and heparin (Lipid) or saline (Control) was administered to eight healthy male subjects on separate occasions for 210 min. Insulin, glucagon and somatostatin were administered from 60 to 210 min in each study and euglycaemia was maintained. 3. Plasma non-esterified fatty acid levels plateaued at 420 +/- 50 mumol/l with the Lipid infusion but were completely suppressed during the Control clamp. Forearm non-esterified fatty acid uptake increased with the Lipid infusion (+50 +/- 10 nmol min-1 100 ml-1 of forearm) and was accompanied by a significant decrease in forearm glucose uptake (+3.23 +/- 0.25 versus +3.65 +/- 0.35 mumol min-1 100 ml-1 of forearm, Lipid and Control, respectively; P less than 0.05) and alanine release (-84 +/- 12 versus -113 +/- 15 nmol min-1 100 ml-1 of forearm, Lipid and Control, respectively; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Acute effects of a somatostatin analogue on kidney function in type 1 diabetic patients.

Suppression of growth hormone by means of somatostatin has been suggested as a possible adjunct therapy in Type 1 diabetes. To assess the acute effect of the somatostatin analogue SMS 201-995 on kidney function in uncomplicated Type 1 diabetes, 13 normoalbuminuric, normotensive diabetic patients were investigated before and during IV infusion of SMS 201-995 (8 micrograms h-1). A control experiment with infusion of carrier only was also performed. The SMS infusion induced a reduction in the glomerular filtration rate (clearance of 125I-iothalamate) and renal plasma flow (131I-hippuran) from 140 +/- 15 (mean +/- SD) and 550 +/- 69 to 131 +/- 14 (2p less than 0.005) and 492 +/- 73 ml min-1 1.73-m-2 (2p less than 0.001), while filtration fraction and total renal resistance rose (both 2p less than 0.001). Urinary albumin excretion rate, blood pressure, and blood glucose concentration were unchanged. Plasma growth hormone and glucagon were significantly suppressed. The reduction in glomerular filtration rate and renal plasma flow correlated with the fall in glucagon concentration (r = 0.57, 2p = 0.04, and r = 0.63, 2p = 0.02). The urinary flow rate was markedly reduced, urine osmolality increased, and fractional excretion of sodium, calcium, and phosphate were reduced. Arginine vasopressin, atrial natriuretic peptide, angiotensin II, and aldosterone were unchanged by the SMS infusion. Thus SMS 201-995 acutely reduces glomerular filtration rate and renal plasma flow in uncomplicated Type 1 diabetes and has an antidiuretic effect. The effects may be related to suppression of glucagon secretion.

Adult↗

PubMed1990

Effects of a growth hormone pulse on total and forearm substrate fluxes in humans.

Under physiological circumstances growth hormone (GH) is secreted in bursts after the onset of sleep and a few hours postprandially. Because most relevant studies have employed constant or repeated infusion of high doses of GH, the possible metabolic effects of such bursts are largely unknown. We have studied seven healthy, male subjects for 7 h after an intravenous bolus of 1) 140 micrograms GH and 2) saline. When injected, serum GH rose to a peak of 21 +/- 3 micrograms/l 10 min after injection. GH caused 1) a rapid, sustained 55% decrease in forearm glucose uptake (P less than 0.05) followed by increases toward control values, 2) a delayed 5 mg/100 ml decrease in plasma glucose (P less than 0.05), and 3) significant 60-250% increases (P less than 0.05) in all measured lipid intermediates (nonesterified fatty acids, 3-hydroxybutyrate, and glycerol) 120-160 min after administration followed by decreases to below control values (P less than 0.05). GH did not influence circulating levels of insulin, C-peptide, glucagon, or insulin-like growth factor I (IGF-I), or isotopically determined glucose turnover. Physiological bursts of GH secretion appear to have acute insulin antagonistic effects with maximal effect on lipolysis after 2 h. These effects are reversed after 4 h. Therefore, GH could play a key role in regulation of diurnal rhythms of substrate levels and fuel utilization in humans.

3-Hydroxybutyric Acid↗

PubMed1990

Evening versus morning injections of growth hormone (GH) in GH-deficient patients: effects on 24-hour patterns of circulating hormones and metabolites.

Since serum GH in normal subjects displays a circadian variation with a major and consistent surge after the onset of sleep we examined whether the time of GH administration in GH-deficient patients had any impact on its action. Eight GH-deficient patients all underwent 3 4-week study schedules in random order: 1) evening (2000 h) sc GH injections, 2) morning (0800 h) sc GH injections, and 3) no GH administration. At the end of each period the patients were admitted to hospital for 24-h measurements of hormones and metabolites. For comparison, 10 age- and sex-matched healthy untreated subjects were hospitalized once under identical conditions. Mean (+/- SE) GH availability, i.e. the area under the curve (AUC; micrograms per L/12 h) for 12 h after injection was significantly greater after evening injection than after morning injections [83.3 +/- 25.4 (evening) vs. 46.0 +/- 10.6 (morning); P less than 0.01]. This might be due to higher skin and sc temperatures when in bed. The 2000-0800 h AUC after evening injection was similar to the corresponding AUC in the reference group. Mean 24-h serum insulin-like growth factor-I levels (micrograms per L) were similar after evening (189.8 +/- 2) and morning (179.5 +/- 5.3) injections (P = 0.8), but the latter displayed a circadian variation suggesting that a steady state had not been reached. Both were significantly lower than the stable reference value (248.4 +/- 3.6 micrograms/L). Blood glucose profiles after morning and evening GH did not differ from that of the reference group, whereas blood glucose decreased when the patients received no GH (P less than 0.01). Daytime (0800-2400 h) insulin levels were increased after morning injections (P less than 0.05). Nighttime levels of lipid intermediates were below normal in the untreated state and after morning injection (P less than 0.05), whereas nighttime blood alanine tended to be above normal after morning GH injection (P = 0.08). Highly significant inverse relationships between circadian lipid intermediates and both blood alanine and lactate concentrations were observed in the reference group and in the patients after evening injections. These relationships disappeared after morning injections. We conclude that the metabolic effects of sc GH injections are clearly influenced by the time of administration and that the closest similarity to normal hormone and metabolite patterns and relationships is reached by GH injection in the evening in GH-deficient patients.

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↗

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 cardiovascular effects of octreotide treatment in acromegaly: an echocardiographic study.

Nine acromegalic patients were treated by the somatostatin analogue SMS 201-995 octreotide (Sandostatin (octreotide), Sandoz, Basle, Switzerland] 250 micrograms/day in 4 divided s.c. injections (50 + 50 + 50 + 100 micrograms) for 1 month, 250 micrograms/24 has continuous s.c. infusions for another month and thereafter 200 micrograms three times daily as s.c. injections. Echocardiography was performed before the treatment, following 1 month of octreotide s.c. infusion/injection and after 6 and 12 months of octreotide treatment. No differences in serum growth hormone, heart rate, blood pressure, cardiac contractility or left ventricular wall mass or wall thickness were found between the infusion and the injection periods. As compared to the pretreatment levels serum growth hormone decreased by 62 and 66% respectively following 6 and 12 months octreotide treatment. The heart rate per minute (+/- SD) decreased from the pretreatment level of 75 +/- 12 to 63 +/- 13 (P less than 0.007) at month 12. The systolic and the diastolic blood pressure decreased from the pretreatment level of 121 +/- 8 and 79 +/- 5 mmHg respectively to 108 +/- 7 (P less than 0.0007) and 71 +/- 7 mmHg (P less than 0.0001) respectively at month 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

PubMed1989

Metabolic and hormonal responses to exogenous hyperthermia in man.

To study whether hyperthermia reproduces hormonal and metabolic responses seen in stress states such as mild infections, six normal male subjects underwent (i) a 3-h hot bath and (ii) a 3-h thermoneutral control period. During the hot bath body temperature rose by 1.2 +/- 0.03 degrees C (mean +/- SEM) and significant peaks of circulating growth hormone (56 +/- 9 vs 7 +/- 4 mU/l), adrenaline (310 +/- 34 vs 152 +/- 39 pmol/l), glucagon (19.2 +/- 4.3 vs 11.8 +/- 2.3 pmol/l) and cortisol were recorded together with slight hyperinsulinaemia (6.5 +/- 1.3 vs 5.3 +/- 1.0 mU/l, P less than 0.05). Hyperthermia was also accompanied by significant increases in circulating levels of free fatty acids (0.93 +/- 0.1 vs 0.46 +/- 0.1 mmol/l), 3-hydroxybutyrate (196 +/- 67 vs 50 +/- 18 mumol/l), glycerol (102 +/- 10 vs 48 +/- 5 mumol/l) and lactate. Blood alanine decreased and blood glucose remained constant. When an intravenous glucose tolerance test was performed during the last hour of hyperthermia signs of impaired first phase and enhanced second phase insulin responses were recorded. Calculated values for glucose disappearance also deteriorated (1.34 +/- 0.19 vs 2.04 +/- 0.50 %/min, P less than 0.05). We conclude that hyperthermia mimics most major metabolic and hormonal changes observed during mild infection and could provide a model to study these conditions.

Adult↗

PubMed1989

Effect of growth hormone dosing on ultimate weight and length of XO mice.

Mice with the karyotype 39, XO and XX mice with the same genetic background were injected for a six month period with daily subcutaneous doses of 0.5 IU biosynthetic human growth hormone (hGH) or with placebo. The XO mice dosed with hGH obtained a significantly higher body weight and greater final length than the XO mice dosed with placebo (39.2 g versus 29.0 g and 21.1 cm versus 19.2 cm respectively). The body weight remained constant after cessation of dosing. The XX mice became significantly longer but not heavier as a result of hGH dosing. The placebo dosed XO mice became significantly longer than the placebo XX mice but their body weights were comparable. Dosing with hGH caused a significant increase in growth rate in both XO and XX mice, and the ultimate body weight was reached within a significantly shorter time period. In the XO mice the hGH injections increased significantly the length and thickness of the femoral bones and the length of the tibia bones. Stimulated endogenous plasma growth hormone levels were significantly higher in XX mice compared to XO mice. Plasma IGF-I levels were significantly higher in XO compared to XX mice, but the levels were not affected by hGH dosing. XO mice may be useful in future metabolic and hormonal studies.

Animals↗

PubMed1989

Influence of growth hormone on glucose-induced glucose uptake in normal men as assessed by the hyperglycemic clamp technique.

To determine whether physiological increments in circulating GH concentrations influence glucose-induced glucose uptake (GIGU), two-step sequential hyperglycemic clamp (plasma glucose, 6 and 14 mmol/L) studies were performed in six normal subjects with and without GH infusion (40 ng/kg.min). The latter resulted in serum GH levels of 15 +/- 1 (+/- SE) microgram/L. Infusion of somatostatin (250 micrograms/h during step 1 and 750 micrograms/h during step 2) together with a replacement dose of insulin (1.1 pmol/kg.min) resulted in serum insulin levels comparable to basal levels in both studies. The GIGU ([3-3H]glucose), assessed as the difference between steps 2 and 1 glucose utilization during the final 60 min of each step (150 min) was markedly impaired during GH infusion (with GH, 1.1 +/- 0.2 mg/kg.min; without GH, 3.1 +/- 0.3 mg/kg.min; P less than 0.001). Moreover, the percent increase in glucose uptake was considerably reduced during hypersomatotropinemia (with GH, 44 +/- 9%; without GH, 97 +/- 11%; P less than 0.01). In the GH infusion as well as control studies, endogenous glucose production (EGP) was similar at the two levels of glycemia, whereas GH infusion approximately doubled EGP [2.3 +/- 0.2 vs. 1.1 +/- 0.3 mg/kg.min and 2.0 +/- 0.4 vs. 1.1 +/- 0.4 mg/kg.min (step 1 and 2, respectively)]. We conclude that moderate hypersomatotropinemia for several hours is characterized by impaired GIGU as well as augmented EGP.

Adult↗

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↗

PubMed1988

Glucagon responses to intravenous arginine and oral glucose in insulin-dependent diabetic patients during six months conventional or continuous subcutaneous insulin infusion.

To elucidate the impact of subcutaneous insulin infusion (CSII) treatment on the glucagon response to intravenous (IV) arginine and to oral glucose a 6-month prospective randomized study in insulin-dependent diabetics was carried out. The effects were investigated of CSII (7-patients) and conventional insulin treatment (UCT) (9 patients) on the changes in glucagon, growth hormone, glucose, lactate, glycerol, 3-hydroxybutyrate, and alanine to IV arginine and to oral glucose in insulin-dependent diabetics who were made euglycemic and isoinsulinemic using the artificial pancreas (Biostator, Miles, Elkhart, IN). HbA1c was significantly lower in the group treated by CSII. Despite the improved glycemic control no significant change in the responses of A-cell secretion to arginine or glucose challenges was found. In addition, there were no significant differences in hormone or metabolite values between the two groups at entry to the study or after 6 months of either therapy. Thus, normalization of the A-cell sensitivity to glucose in insulin-dependent diabetic subjects requires further amelioration of the intermediary metabolism than can be achieved with insulin pump treatment.

Administration, Oral↗

PubMed1988

Growth in young rats after termination of sodium selenite exposure: studies of growth hormone and somatomedin C.

In a previous study we have shown that the growth retarding effect of selenium in infant rats occurs concomitantly with severely reduced growth hormone responses and serum somatomedin C. Furthermore, normal growth may be restored by administration of exogenous growth hormone administration. In the present study we examined the alterations after withdrawal of selenite administration in growth rate, serum growth hormone after GRF 40 injection and serum somatomedin C. Thirty-six rats were divided into 3 groups; i.e. controls, rats on continuous selenite treatment from days 21 to 63 of age and a group where selenium was withdrawn on day 42. The first 2 groups grew linearly during the experimental period, the second at a very significantly lower rate. In the third group after cessation of exposure a brief growth spurt occurred followed by a growth rate significantly different from that of the other 2 groups. The reduced GH response to GRF 40 stimulation was normalized 3 weeks after withdrawal, whereas serum somatomedin C remained at the same low level as in those rats on continuous selenite administration. There were other signs of liver lesion at day 42, i.e. elevated ALAT and reduced serum albumin, changes which became insignificant in all 3 groups at the end of the experiment. These results demonstrate that whereas stimulated growth hormone secretion was reestablished 3 weeks after termination of selenium exposure, severely reduced liver somatomedin C production persisted. An improvement in growth rate was also noted, but normal growth rate was not reached 3 weeks after discontinuation of the selenite treatment.

Age Factors↗

PubMed1988

A hyperkinetic heart in uncomplicated active acromegaly. Explanation of hypertension in acromegalic patients?

Cardiac function was studied by echocardiography in 12 patients with active acromegaly and in 12 age- and sex-matched healthy control subjects. None of the patients had cardiovascular diseases or other endocrine diseases than acromegaly. The patients had a mean age of 39 +/- 5 years and were short-term acromegalic with a mean duration of disease of 6 +/- 3 years. Mean left ventricular mass was 163 +/- 43 g/m2 in the acromegalic group versus 120 +/- 24 g/m2 in the control group. Preload (the diastolic diameter of the left ventricle) was within normal limits, while afterload (end-systolic meridional wall stress) was significantly decreased in the acromegalic group. Myocardial contractility assessed as fractional shortening of the left ventricle was 39.9 +/- 3.6% in the acromegalic group versus 32.9 +/- 5.1% in the control group, and cardiac output was increased by 52% in the acromegalic group because of increased heart rate and stroke volume. We suggest that augmented peripheral blood flow is responsible for the condition of cardiac hyperkinesia in short-term acromegaly and involved in the development of hypertension, which is a frequent complication of long-term acromegaly.

Acromegaly↗

PubMed1988

Marked impairment of the effect of hyperglycaemia on glucose uptake and glucose production in insulin-dependent diabetes.

The effect of hyperglycaemia per se on glucose utilization and glucose production was evaluated in 12 patients with insulin-dependent diabetes and in 9 non-diabetic control subjects. In diabetic patients normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin infusion. During the study endogenous insulin secretion was suppressed by somatostatin (300 micrograms h-1) and replaced by infusion of insulin (0.2 mU kg-1 min-1). Glucose utilization and hepatic glucose production rates were quantified at two plasma glucose concentrations (6.7 and 16.7 mmol l-1) using the two-step sequential hyperglycaemic clamp technique in combination with 3-3H-glucose tracer infusion. Duration of each step was 120 min. In diabetic patients glucose utilization, at a glucose concentration of 6.7 mmol l-1, was not different from normal (mean +/- SE: 2.9 +/- 0.2 vs 3.6 +/- 0.3 mg kg-1 min-1, 0.05 less than p less than 0.10), but the response to marked hyperglycaemia was significantly reduced (5.4 +/- 0.5 vs 9.4 +/- 1.0 mg kg-1 min-1, p less than 0.01). Hepatic glucose production was also normal at 6.7 mmol l-1 (1.4 +/- 0.1 vs 1.4 +/- 0.1 mg kg-1 min-1, NS), but whereas in control subjects glucose production was suppressed during hyperglycaemia of 16.7 mmol l-1 (0.3 +/- 0.4 mg kg-1 min-1, p less than 0.01), a slight increase was observed in diabetic patients (2.0 +/- 0.2 mg kg-1 min-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Dose-response studies with biosynthetic human growth hormone (GH) in GH-deficient patients.

Increasing doses of biosynthetic human GH (R-hGH) were given sc to seven GH-deficient patients for three consecutive 14-day periods (2, 4, and 6 IU/day at 2000 h), followed by 14 days of no GH therapy. At the end of each period each patient was hospitalized for frequent blood sampling from 2000 to 1100 h the following day. A dose-dependent increase in serum GH and serum insulin-like growth factor I (IGF-I) levels occurred. However, the time course of the serum IGF-I concentrations was different on the four occasions; there was a significant fall in the evening when no therapy was given (P less than 0.01), a significant increase after injections of 2 IU R-hGH, and constant levels during treatment with 4 and 6 IU R-hGH. Plasma glucose levels were within the normal range, with a significantly lower fasting level (at 0400 h) when no GH was given. Breakfast induced a plasma glucose rise when GH was administered, but no rise without GH, and a postprandial serum insulin response that was GH dose dependent. GH therapy increased serum FFA (P less than 0.05) and blood 3-hydroxybutyrate levels, but had no effect on blood alanine or lactate or serum triglyceride and cholesterol levels. We conclude that the serum IGF-I response to GH is dose dependent, and that a GH replacement dose of 2 IU/day (equalling 1.5 IU/m2.day) is insufficient to maintain normal diurnal serum IGF-I levels. Furthermore, a GH-independent diurnal variation in serum IGF-I in these patients is suggested. This GH preparation also has diabetogenic and lipolytic actions.

3-Hydroxybutyric Acid↗

PubMed1988

Growth hormone restores normal growth in selenium-treated rats without increase in circulating somatomedin C.

Selenium intake (5.0 ppm) induces growth retardation, accumulation of selenium in somatotrophs, lack of growth hormone response to GHRH and an 80 per cent reduction in serum somatomedin C in infant rats. In addition, it induces a slight reduction in serum albumin and occasionally slight central liver necrosis. In order to determine the role of insufficient growth hormone production, the influence of exogenous growth hormone was studied during selenium intake in groups of rats during 25 to 46 days of age (post-weaning). A dosage of human growth hormone (100 micrograms twice daily) was chosen, this being sufficient to restore normal growth rate and normal serum somatomedin C in hypophysectomized rats of similar age. The weight gain in selenium-treated (3.3 ppm) rats was 46.0 +/- 11.7 g (SD)/21 days, whereas in selenium rats given growth hormone it was 66.6 +/- 8.9 g (P = 0.01), which was similar to the gain in control rats 72.3 +/- 6.9 g. The latter two were less than the weight gain in control rats given growth hormone: 91.5 +/- 11.5 g (P = 0.01 and P less than 0.01). Serum somatomedin C in untreated rats was 151 +/- 66 (SD) micrograms/l (25 days) increasing to 532 +/- 91 micrograms/l (34 days) and 482 +/- 64 micrograms/l (46 days). It did not increase above these levels in control rats given growth hormone. In selenium-treated rats, no increase occurred during growth hormone administration 138 +/- 148 micrograms/l (34 days) and 185 +/- 84 micrograms/l (46 days) (P less than 0.001 and P less than 0.001 vs untreated controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗