Biomedical subjects

A Skottner

Publications and source records attributed to A Skottner.

At least 55 records · Page 3Linked to original sources

PubMed1990

Acute effects of insulin-like growth factor I and insulin on glucose metabolism in vivo.

We have compared the actions of insulin-like growth factor (IGF-I) and insulin on glucose metabolism in vivo, using the glucose clamp technique in rats. Both hormones caused dose-dependent inhibition of hepatic glucose production, stimulation of whole body glucose disposal, and an increase in the glucose metabolic rate of specific muscles. Infusion of IGF-I also decreased the plasma concentration of insulin. An an infusion rate of 0.57 nmol.kg-1.min-1, IGF-I led to stimulation of whole body glucose uptake that was similar to the glucose uptake produced by infusion of 0.01 nmol.kg-1.min-1 insulin. The glucose metabolic rate, as measured by 2-deoxy-D-glucose uptake, was comparable in quadriceps femoris, soleus, and diaphragm muscles during the infusion of 0.57 nmol.kg-1.min-1 IGF-I and 0.01 nmol.kg-1.min-1 insulin. However, at these rates of infusion, IGF-I caused only a 38 +/- 6% inhibition of hepatic glucose output compared with 66 +/- 12% inhibition by insulin (P less than 0.05). Thus, under these conditions, muscle is more responsive than liver to IGF-I, which agrees with the complement of IGF-I receptors in the two tissues.

Animals↗

PubMed1990

Differential effects of IGF-I and insulin on glucoregulation and fat metabolism in depancreatized dogs.

The effects of equipotent glucose-lowering doses of insulinlike growth factor I (IGF-I) and insulin on tracer-determined glucose kinetics and several metabolites were compared in 14 experiments (7 in each group) in fasted, totally depancreatized dogs. This model prevented variations in insulin secretion induced by IGF-I and permitted evaluation of the effects of IGF-I on extrapancreatic glucagon. Steady-state moderate hyperglycemia (9.9 +/- 0.2 mM) was maintained by a subbasal intraportal infusion of insulin (1.29 +/- 0.17 pmol.kg-1.min-1). This was continued throughout the experiment, allowing evaluation of IGF-I effects on insulin clearance. Human recombinant IGF-I or insulin was given intravenously as a primed infusion for 90 min, followed by a 50-min recovery period. The dose of IGF-I was a 2.6-nmol/kg bolus plus 57.4 pmol.kg-1.min-1. The insulin dose required to induce the same plasma glucose decline as IGF-I (44 +/- 6 vs. 43 +/- 5%, NS) was 9-12 times lower (0.06-nmol/kg bolus + 6.4 +/- 0.6 pmol.kg-1.min-1). However, the mechanism of this decline differed with IGF-I and insulin; glucose production was much less suppressed (25 +/- 9 vs. 42 +/- 11%, P less than 0.001) and glucose utilization was more stimulated (68 +/- 18 vs. 38 +/- 19%, P less than 0.05) with IGF-I.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Nerve regeneration and serum levels of insulin-like growth factor-I in rats with streptozotocin-induced insulin deficiency.

Peripheral nerve regeneration was studied in female Sprague-Dawley rats with streptozotocin-induced insulin deficiency. Nerve regeneration was provoked by a crush lesion on the sciatic nerve 21 days after the streptozotocin injection. The regeneration was assessed by a pinch test at different time-points after injury. The rate of regeneration in insulin-deficient animals, 2.5 mm/day, was significantly lower than in control animals, 2.9 mm/day (P less than 0.05). There was no difference in the initial delay, i.e. the period before regeneration attains a constant velocity. One group of insulin-deficient rats was treated with insulin during the regeneration period by means of implanted osmotic mini-pumps. This treatment prevented the decrease in regeneration. After 6 days the sciatic nerves of insulin-deficient rats had regenerated 12.3 +/- 0.3 mm (mean +/- S.E.M.), while the corresponding value for insulin-treated rats was 15.7 +/- 0.6 mm. (P less than 0.01). The streptozotocin-treated rats were found to have a 39% reduction in the serum level of insulin-like growth factor-I (IGF-I) compared to control rats (0.33 +/- 0.02 micrograms/ml and 0.54 +/- 0.02 micrograms/ml respectively, P less than 0.001). Insulin treatment during the regeneration period completely restored the IGF-I level back to normal.

Animals↗

PubMed1989

Isolation and characterization of a glycosylated form of human insulin-like growth factor I produced in Saccharomyces cerevisiae.

Expression and secretion of human insulin-like growth factor-I (IGF-I) in Saccharomyces cerevisiae was achieved by linking an actin (ACT) promoter to an MF alpha 1 prepro leader peptide/IGF-I gene fusion. Purified human IGF-I from yeast culture media was found to contain, in addition to the native form, also a glycosylated variant. Structural studies showed that both IGF-I forms were processed identically, resulting in 70-amino-acid long polypeptides, with intact N-terminal and C-terminal residues of glycine and alanine, respectively. The glycosylation site was determined to threonine-29 (Thr29), by 1H NMR spectroscopy and protein sequence analysis of an isolated tryptic peptide(22-36). No other glycosylation sites were found. Only mannose was detected in the sugar analysis, with an estimated content of 4.5% w/w corresponding to 2 mannose residues per molecule of IGF-I. The carbohydrate structure, determined by 1H and 13C NMR spectroscopy, was found to be alpha-D-Manp(1----2)alpha-D-Manp(1----3)Thr corresponding to an O-linked glycoprotein structure. No other post-translational modifications could be identified in the glycosylated IGF-I form. Furthermore, this form was highly active, comparable to native IGF-I, exhibiting a specific activity of 20,500 units/mg, as determined by a radio-receptor assay.

Actins↗

PubMed1989

Insulin-like growth factor I (IGF-I) stimulates regeneration of the rat sciatic nerve.

The effect of insulin-like growth factor I (IGF-I) was tested on regeneration of the rat sciatic nerve after a crush lesion. IGF-I was administered via miniosmotic pumps to the dorsal root ganglia or locally around the crush lesion. Regeneration of sensory fibers was measured after 3 or 4 days superfusion by pinching. IGF-I stimulated regeneration in both administration paradigms. Regeneration was inhibited if the nerve was perfused with specific antibodies to native IGF-I. The results suggest that endogenous extracellular IGF-I plays an important role during regeneration of peripheral nerve fibers.

Animals↗

PubMed1989

Somatomedin C in the pancreas of young and adult, normal and obese, hyperinsulinemic mice.

Immunocytochemical, immunochemical and RNA-hybridization techniques were used to map the distribution of somatomedin C (Sm-C; insulin-like growth factor I; IGF-I) in the pancreas of young and adult lean and obese mice. The D cells in the islets of Langerhans showed intense cytoplasmic Sm-C immunoreactivity, extending into their processes. Only slight Sm-C immunoreactivity was seen in A and B cells, apparently confined to the plasma membranes. In the exocrine pancreas scattered duct cells were immunopositive. Starvation increased, while feeding decreased the Sm-C immunoreactivity in B cells. RNA-hybridization analyses revealed that roughly the same number of Sm-C mRNA molecules, as calculated per DNA amount in the pancreas, could be demonstrated in young and adult, lean and obese mice. Radioimmunoassay (RIA) determinations of total Sm-C showed that there were about equal concentrations in the pancreas of lean and obese mice. There were marked differences between the liver and the pancreas, in that the RIA Sm-C values for the former were twice those in the latter while, in contrast, the corresponding values for the Sm-C mRNA, i.e. the agent determining the synthesis of Sm-C, were about 100 times higher in the liver as compared to that in the pancreas. We interpret our results as follows: The D cells in the islets form and secrete Sm-C in both young and adult, lean and obese mice, while A and B cells bind, but do not necessarily synthesize this peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Circulating insulin-like growth factor I in type 1 (insulin-dependent) diabetic patients with retinopathy.

The relationship between insulin-like growth factor I (IGF I) and diabetic retinopathy was investigated. This somatomedin circulates bound to at least two large carrier proteins with molecular weights of approximately 150,000 and 35,000. Total and protein binding profiles of insulin-like growth factor I were determined in the serum of 18 patients who had had Type 1 (insulin-dependent) diabetes for 15-20 years, but had no signs of nephropathy and a similar degree of mild subclinical neuropathy. Nine had preproliferative or proliferative retinopathy and 9 had little or no background retinopathy but there was no difference in diabetes duration, insulin doses or glycaemic control between the two groups. In the latter group, the amounts of the somatomedin I and the serum profiles were similar to those in 9 healthy control subjects. In patients with advanced retinopathy, however, binding of insulin-like growth factor I to the carrier proteins was significantly altered. Binding to the low molecular weight protein increased to 140% whereas binding to the large molecular weight protein decreased to 70% of the normal level. In the latter Type 1 diabetic patients total serum insulin-like growth factor I was decreased to 60% of the normal level (p less than 0.02). When the alteration in serum profile was adjusted for, the level of somatomedin associated with the small carrier complex was normal whereas that associated with the large carrier complex was reduced by almost 60% in Type 1 diabetic patients with retinopathy. It is proposed that the total circulating somatomedin level is low in advanced diabetic retinopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Muscle regeneration. The effect of hypophysectomy on cell proliferation and expression of insulin-like growth factor-I.

Against the background of the importance of growth hormone (GH) for normal muscle growth, a study was performed to investigate whether lack of GH after hypophysectomy affects the cell proliferation and the local production of insulin-like growth factor-I (IGF-I) in the early stages of muscle regeneration in adult rats. The level of IGF-I in the serum of hypophysectomised rats was reduced to about 30% of that of controls. The incorporation of [methyl-3H]thymidine into the regenerating muscle showed a peak 6 days after the operation and then gradually declined to the end of the period of study 30 days after initiation of regeneration by ischemic necrosis. The DNA content rose to a maximum level after 6-8 days, and remained high after 30 days. There was no major difference in the incorporation of [3H]thymidine in regenerating muscle of hypophysectomised and control rats, but the DNA concentration in the regenerating muscles of hypophysectomised rats was significantly reduced after 30 days. There was a corresponding reduction in the number of nuclei per muscle fibre, indicating that hypophysectomy has a small effect on the cell proliferation during the early stages of muscle regeneration. Immunohistochemical demonstration of IGF-I in the regenerating muscle revealed the transient presence of immunoreactive material in satellite cells and myotubes after 6 to 8 days of regeneration but no immunoreactivity after 30 days. No obvious difference was observed between hypophysectomised and control rats, indicating that the endogenous production of IGF-I in regenerating skeletal muscle can occur independently of GH.

Animals↗

PubMed1989

Binding of insulin-like growth factor-I (IGF-I) to primary cultures of chondrocytes from rat rib growth cartilage.

Binding of insulin-like growth factor I (IGF-I) to cultured resting, proliferative and hypertrophic growth plate chondrocytes was investigated. The optimal binding conditions and the extent of degradation of the 125I-IGF-I at 20 degrees C were analyzed in a time-course study. The maximal binding without noticeable degradation was observed after 3 h. The binding of IGF-I to the proliferative cells was 2-fold higher than to the resting and the hypertrophic cells. On the proliferative chondrocytes two classes of receptors with different affinities were found. 125I-IGF-I could be displaced from the proliferative cells by unlabelled IGF-I, IGF-II and insulin, respectively. Half maximal binding was observed at 0.3 nmol/l (= 2.2 micrograms/l) of IGF-I, 4.3 nmol/l (= 32 micrograms/l) of IGF-II and 350 nmol/l (= 2000 micrograms/l) of insulin. No specific binding of human growth hormone (hGH) could be demonstrated. When binding of epidermal growth factor (EGF) to the proliferative cells was assessed, little, but specific binding was observed.

Animals↗

PubMed1989

Effects of growth hormone on skeletal muscle. II. Studies on regeneration and denervation in adult rats.

The effects of human recombinant growth hormone (rhGH) on regenerating skeletal muscle after ischaemic necrosis and on denervated skeletal muscle were studied in normal adult rats. One group of rats was treated with 4 IE rhGH daily by subcutaneous injections, while control rats were injected with saline. The treatment with rhGH resulted in increased levels of insulin-like growth factor-I (IGF-I) in serum. Ischaemic necrosis was achieved in the extensor digitorum longus (EDL) muscle by cutting the supplying vessels and nerve fascicles at the entrance into the muscle. The wet weight and DNA: protein ration in the regenerating muscle were determined 2 and 4 weeks after the operation. The weight of the regenerating muscles in the rats treated with rhGH during the period of study was larger than in the control rats, while the DNA:protein ratio did not differ significantly between the groups. Denervation of the EDL and soleus muscles followed by subsequent reinnervation was obtained by freezing the sciatic nerve with a forceps chilled in liquid nitrogen. Rats treated with rhGH during the period of denervation and reinnervation, i.e. during the 4 weeks after the freezing of the sciatic nerve, revealed increased weight of both the reinnervated and normal muscles compared to corresponding muscles of control rats. Denervation of the EDL and soleus muscles without subsequent reinnervation was achieved by cutting the sciatic nerve at the level of the thigh. Four weeks after denervation the muscles showed atrophy, mainly affecting type 2 fibres in the EDL muscle and both type 1 and type 2 fibres in the soleus muscle.

Adenosine Triphosphatases↗

PubMed1989

Growth responses in a mutant dwarf rat to human growth hormone and recombinant human insulin-like growth factor I.

A new mutant GH-deficient dwarf rat has been used to study the effects of iv infusions of human GH (hGH) and recombinant human insulin-like growth factor I (hIGF-I). This animal has only about 5% of normal pituitary GH content, low circulating GH levels, and no regular GH surges. The defect seems to be specific for GH. Infusions of hIGF-I at 180 micrograms/day for 9 days elevated serum IGF-I concentrations significantly over those in the saline-infused controls (713 +/- 20 ng/ml vs. 395 +/- 31 ng/ml); hGH infusions did not raise IGF-I levels significantly (435 +/- 20 ng/ml). Gel filtration of serum samples showed that the high-dose hIGF-I infusions increased free IGF concentrations, without apparently altering the pattern of IGF-I binding whereas hGH infusions increased the amount of high mol wt IGF-I binding protein. Neither IGF-I nor hGH infusions affected the small amounts of rat GH present in the dwarf rat pituitary glands. Continuous iv infusions of hGH (200 mU/day for 9 days) stimulated body wt gain (2.1 +/- 0.2 g/day) and bone growth (96 +/- 9 microns/day) significantly compared to saline-infused dwarf rats (1.2 +/- 0.3 g/day and 43 +/- 3 microns/day). Infusions of hIGF-I at 180 micrograms/day produced a body wt gain (2.1 +/- 0.5 g/day) similar to that seen in the hGH-infused group but a significantly smaller stimulation of bone growth (63 +/- 3 microns/day). Infusion of a 5-fold lower dose of hIGF-I (36 micrograms/day for 9 days) had no effect on body wt or bone growth. Food intake was unaffected by either hGH or hIGF-I infusions. The pattern of tissue growth was affected differentially by hGH and IGF-I infusions that produced the same overall body wt gain. hGH induced a relatively proportional growth in most of the organs studied, whereas hIGF-I infusion at 180 micrograms/day stimulated a disproportionately greater growth of the kidney, adrenals, and spleen. In some of the animals, tissues were extracted for RIA of IGF-I; the amounts of IGF-I in the liver were similar in control, hGH, or IGF-I-infused animals, whereas kidney and adrenals from IGF-I infused animals contained larger amounts of immunoreactive IGF-I than did those tissues from hGH-treated rats. Thus, both hGH and hIGF-I can promote growth in the mutant dwarf rat, but they differ both quantitatively and qualitatively in their pattern of actions.

Animals↗

PubMed1989

Growth hormone and growth in diabetic rats: effects of insulin and insulin-like growth factor-I infusions.

The effects of streptozotocin-induced diabetes on weight gain, bone growth and GH secretion have been studied in conscious chronically cannulated male rats. In addition to the classic diabetic symptoms (hyperphagia, polydipsia, polyuria, glycosuria and hyperglycaemia), the slow body weight gain (0.95 +/- 0.5 compared with 2.63 +/- 0.5 g/day in non-diabetic controls) was associated with a reduction in bone growth (from 162 +/- 9 to 48 +/- 4 microns/day) and a reduced pituitary GH content (from 1.5 +/- 0.2 to 0.6 +/- 0.06 mg/gland). Serial blood sampling during the day or overnight showed that the normal male episodic GH secretory pattern was obliterated in the diabetic animals. The constant osmotic stimulation of hyperglycaemia and high fluid turnover was reflected in a significant reduction in pituitary oxytocin and arginine vasopressin (AVP) stores. Intravenous insulin infusions (67-1340 pmol/h for 4 or 7 days) caused a large initial weight gain (greater than 20 g in 2 days) followed by a slower increase, and stimulated tibial bone growth (to 100 +/- 16 and 126 +/- 8 microns/day after 4 or 7 days respectively). Insulin infusion for 7 days also increased pituitary GH content (to 1 +/- 0.15 mg/gland), and the normal episodic GH secretory pattern returned. Intravenous infusions of insulin which reduced, but did not completely normalize, blood glucose levels, allowed the resumption of growth and pulsatile GH secretion. Continuous infusion of recombinant human insulin-like growth factor-I (hIGF-I) at 1110 pmol/h for 54 h also caused a large initial rise in body weight in diabetic rats (17.1 +/- 1.6 compared with 7.5 +/- 2.8 g in saline-infused controls) due primarily to increased fluid retention. This effect of hIGF-I occurred without any significant changes in pituitary GH, AVP, oxytocin, blood glucose or bone growth over this short-term infusion, nor was there any obvious effect on spontaneous GH secretion, monitored over the entire infusion period. We conclude that the diabetic rat is not a good model to study growth stimulation by short-term insulin or IGF-I treatments because the insulin-like effects of these peptides obscure their specific growth-promoting activities in this model.

Animals↗

PubMed1988

Effects of growth hormone treatment on the regeneration of rat sciatic nerve.

The effect of human growth hormone (hGH) on regeneration of neuronal tissue have been studied in rats. A crush lesion was made on the sciatic nerve at the thigh level in intact or hypophysectomized rats. The hGH was administered systemically via subcutaneously implanted miniosmotic pumps. Regeneration was evaluated by the 'pinch-test' after 3, 4 and 6 days. Regeneration was significantly (P less than 0.05) impaired in hypophysectomized rats, but restored to normal after treatment with hGH (200 mIU/day). In intact rats treatment with 400 mIU/day hGH significantly (P less than 0.05) stimulated regeneration, whereas no effect was observed at 200 mIU/day. Immunoreactive insulin-like growth factor 1 (IGF-1) decreased in hypophysectomized rats, but rose again after hGH treatment. However, no consistent correlation between circulating IGF-1 and the rate of regeneration was found. Our results show that hGH can increase the rate of regeneration in peripheral nerves after injury. This can be due either to direct effects of hGH or to indirect effects via locally produced growth factors (e.g. somatomedins).

Animals↗

PubMed1988

Immunohistochemical localization of insulin-like growth factor I in the adult rat.

Rabbit antisera against native human insulin-like growth factor I (IGF-I; somatomedin C) or a synthetic tetradecapeptide, representing the carboxyterminal amino acids 57-70 of human IGF-I, were used to map immunohistochemically the distribution of IGF-I immunoreactive material in adult rats. Both antisera were specific for IGF-I, as characterized by immunoabsorption, immunoblotting and radioimmunoassay. There was no cross-reactivity to IGF-II, relaxin or pro-insulin; substances having a high degree of structural homology with IGF-I. High IGF-I immunoreactivity was observed in spermatocytes of the testis; in oocytes, granulosa and theca interna cells of the ovary during early stages of follicle development; in some lymphocytes and in reticular cells of lymphoid and hematopoietic organs; in salivary gland duct cells; in the adrenal medulla, the parathyroid gland and the Langerhans' islets. Chondrocytes in the epiphyseal and rib growth plates and at articular surfaces showed strong IGF-I immunoreactivity. Brown but not white fat cells were stained. Nerve cells in the peripheral and autonomic nervous system showed faint to intense IGF-I immunoreactivity. In contrast, neurons and neuroglial cells in the central nervous system were generally negative; motor neurons being an exception. Erythropoietic, thrombocytopoietic and myeloic cells in the bone marrow showed IGF-I immunoreactivity, but only at defined developmental stages. Hepatocytes showed faint IGF-I immunoreactivity, but became more intensely stained after pretreatment with colchicine. The present results suggest that IGF-I is synthetized by cells in several tissues and organs in the adult rat. There was an apparent association between the localization of IGF-I and cell differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Transient increase in insulin-like growth factor I immunoreactivity in rat peripheral nerves exposed to vibrations.

Hind legs of adult rats were exposed to vibrations (81 Hz; amplitude 0.50 mm peak to peak) for 4 h during two consecutive days. The sciatic, tibial and plantar nerves were isolated and processed for immunohistochemical demonstration of IGF-I (insulin-like growth factor I; somatomedin C) immunoreactivity at different time intervals after the vibration exposure. In sham-exposed rats the axons in peripheral nerves showed no or faint IGF-I immunoreactivity while most Schwann cells were negative. Exposure of the hind legs to vibrations induced increased IGF-I immunoreactivity in the Schwann cells, demonstrable at the end of the exposure period and reaching maximal intensity 2-3 days after vibration exposure. Several distended axons similarly showed increased staining. The IGF-I immunoreactivity decreased after 7-10 days to almost the level in the control nerves. The most extensive changes were observed in the plantar nerves. The tibial nerves similarly expressed strongly increased IGF-I immunoreactivity in their Schwann cells. The sciatic nerve showed, however, only slightly to moderately increased staining. Cells in the epineurium of the plantar and, to a limited extent, of the tibial nerves expressed concomitantly increased IGF-I immunoreactivity. We conclude that the transiently increased IGF-I immunoreactivity in peripheral nerves reflects reactive changes caused by vibrations and most prominently expressed by the Schwann cells.

Animals↗

PubMed1988

Differing expression of insulin-like growth factor I in the developing and in the adult rat cerebellum.

Insulin-like growth factor I (IGF-I; somatomedin C) is a trophic peptide of importance for the development of several tissues and organs. In the present study we have mapped the cellular distribution and dynamic changes of IGF-I immunoreactivity in the rat cerebellum from its postnatal development to maturity. In vitro hybridization of IGF-I mRNA was used to demonstrate that the IGF-I immunoreactive material was synthesized in the cerebellum during a limited time period of cerebellar differentiation. IGF-I immunoreactivity was absent in primordial nerve cells but was present in neuroglial cells during the first two days after birth and then rapidly increased in intensity in the latter during the next few days. Proliferative nerve cells in the external granular layer did not express IGF-I immunoreactivity, while migrating and differentiating nerve cells as well as neuroglial cells showed intense labelling. Starting about 2 weeks postnatally, the IGF-I immunoreactivity declined, first in the neuroglial cells and eventually in the nerve cells. No IGF-I immunoreactivity could be demonstrated in the normal adult cerebellum. Colchicine pretreatment did, however, enable demonstration of IGF-I immunoreactivity in adult cerebellar nerve cells but not in neuroglial cells. In vitro hybridization revealed IGF-I mRNA in the developing cerebellum but only at very low levels in the adult cerebellum. It is concluded that IGF-I is likely to be a factor of importance for the development and maturation of nerve cells and neuroglial cells in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1988

Insulin-like growth factor I in the pancreas of normal and diabetic adult rats.

Insulin-like growth factor I (IGF-I, somatomedin C) was mapped by immunocytochemistry in the pancreas of normal and experimentally influenced rats. The polyclonal IGF-I antiserum K 37 was characterized and demonstrated to be specific. In the exocrine pancreas some duct cells showed IGF-I immunoreactivity, other components being negative. The three main endocrine cell types in the islets of Langerhans were IGF-I immunoreactive, most strikingly the D cells. Hypophysectomy resulted in loss of IGF-I immunoreactivity in all three endocrine cell types, i.e. D, A and B cells, while the levels of somatostatin, glucagon and insulin, respectively, remained unchanged. Starvation seemed to increase and feeding to decrease the IGF-I immunoreactivity in the B cells. Cysteamine pre-treatment reduced the normally intense IGF-I and somatostatin immunoreactivities in the D cells. In rats made diabetic with alloxan or streptozotocin, the B cells were irreversibly damaged and lost both their insulin and IGF-I immunoreactivities, while the IGF-I immunoreactivity was increased in A cells; the D cells remained unchanged. The concentrations of IGF-I mRNA in the pancreas were almost equal in normal and alloxan diabetic rats as were the concentrations of extractable IGF-I. We conclude that IGF-I immunoreactive material can be demonstrated in adult animals in all endocrine islet cells, most prominently in the D cells. The expression of IGF-I immunoreactivity is in part under pituitary control. In the adult rat only one islet cell type synthesizes IGF-I immunoreactive material, i.e. the D cells, while, in contrast, the B cells are likely to be a major IGF-I source in fetal and neonatal islets.

Animals↗

PubMed1988

The effects of biosynthetic insulin-like growth factor-1 supplementation on somatic growth, maturation, and erythropoiesis on the neonatal rat.

Somatomedins are anabolic hormones that may stimulate growth during the perinatal period. To test this hypothesis, neonatal rats were injected with a biosynthetic somatomedin, insulin-like growth factor 1 (IGF-1) twice daily for the first 2 wk of life. Two biosynthetic IGF-1 preparations of different potency were tested as well as a preparation of human growth hormone in five litters of rats. When compared to saline-injected rats, IGF-1 injected rats had increased body weight and tail length as well as specific increases in weights of liver, brain, heart, and testes. In addition, significant increases in bone marrow erythropoietic cell precursors were apparent after IGF-1 injection. IGF-1-treated neonatal rats also exhibited precocious eye opening as a sign of epithelial cell differentiation. Five additional litters of rats received similar injections but were exposed to postnatal nutritional deprivation via artificially increasing litter size. Although IGF-1 caused stimulation of bone marrow erythropoiesis and precocious eye opening, no effects of IGF-1 on somatic or organ growth could be documented. This represents the first demonstration in vivo of the anabolic effects of IGF-1 in rapidly growing neonatal rats but suggests that nutritional sufficiency may also be necessary for the full expression of somatomedin effects.

Animals↗