bluuebunny/crossref_metadata_2025_split huggingface dataset:
Potential mechanism of insulin resistance in ageing: impaired insulin-stimulated glucose transport due to a depletion of the intracellular pool of glucose transporters in Fischer rat adipocytes
Authors: Matthaei S. , Benecke H. , Klein H. H. , Hamann A. , Kreymann G. , Greten H. 
Published: December 2008

ABSTRACT
To examine the cellular mechanism responsible for impaired insulin action in ageing, we determined various in-vitro parameters involved in the pathogenesis of insulin resistance, i.e. basal and insulin-stimulated [14C]3-O-methylglucose transport (30MG), 125I-labelled insulin binding, activation of insulin receptor kinase (IRKA) in intact cells, and number and subcellular distribution of glucose transporters in subcellular membrane fractions of adipocytes from 6- (FR-6) and 24- (FR-24) month-old Fischer rats. Ageing had no effect on basal 30MG (12±4 vs 13±3 fmol/5 × 104 cells, means ± s.e.m.); in contrast, in FR-24 rats insulin-stimulated 30MG was markedly decreased by 43% when compared with that in FR-6 rats (158±14 vs 90±8 fmol/5 × 104 cells; P < 0·01). Insulin binding to adipocytes from FR-6 rats was 2·40±0·38% compared with 2·28±0·47% in FR-24 (P not significant). Moreover, ageing had no significant effect on IRKA, as determined by insulin-stimulated (0, 1, 4 and 500 ng insulin/ml) 32P-incorporation into histone 2B. In subcellular membrane fractions, low density microsomes and plasma membranes, glucose transporter numbers were determined using [3H]cytochalasin B binding and immunodetection using an antiserum against the C-terminal peptide of the hepatoma-G2-glucose transporter. Cytochalasin B binding revealed that in the basal state the intracellular pool of glucose transporters was depleted in FR-24 by about 39% compared with low density microsomes from FR-6: (48·6±7·2 vs 29·8±5·5 pmol/mg membrane protein; P < 0·01). In consequence, in FR-24 there were fewer glucose transporters available for insulin-induced translocation to the plasma membrane (insulin-treated plasma membrane: 23·9±4·2 (FR-6) vs 14·4±3·1 (FR-24) pmol/mg membrane protein; P < 0·01). These results were confirmed by immunoblotting.
In conclusion, (1) maximal insulin-stimulated 30MG was decreased by 43% in cells from FR-24 rats compared with those from FR-6 rats, while basal 30MG was similar in both groups, (2) neither insulin binding nor IRKA were significantly altered in cells from FR-24 rats, and (3) impaired insulin-stimulated 30MG was associated with reduced numbers of glucose transporters in the plasma membrane as a consequence of a depletion of the intracellular pool of glucose transporters in cells from FR-24 rats.
Journal of Endocrinology (1990) 126, 99–107
Purification and structural characterization of ovine placental lactogen
Authors: Warren W. C. , Liang R. , Krivi G. G. , Siegel N. R. , Anthony R. V. 
Published: December 2008

ABSTRACT
Discrepancies exist in the reported purity and biological activity of ovine placental lactogen (oPL), and little structural characterization has been reported. Ovine PL was purified from fetal cotyledonary tissue (day 100 of gestation) by monitoring activity with a recombinant bovine GH (bGH) liver radioreceptor assay. Two hundred grams of tissue yielded 4·2 mg of oPL, with an ∼ 1000-fold purification of oPL specific activity following initial tissue extraction. The oPL was radioiodinated and used in an ovine fetal liver (day 100 of gestation) radioreceptor assay to examine competitive displacement of oPL, ovine GH (oGH) and ovine prolactin (oPRL). The potency of oPL (ED50 = 0·18 nmol/l; ED50 is the quantity of ligand necessary to displace 50% of specifically bound 125I-labelled oPL) was greater than that of oGH (ED50 = 4·1 nmol/l) and oPRL (ED50 = 1·1 μmol/l) in competing for 125I-labelled oPL-binding sites.
Attempts to sequence the NH2 terminus of oPL by vapour-phase sequencing indicated that the NH2 terminus was blocked. Purified oPL was subjected to trypsin and CnBr digestion, and two CnBr and six tryptic peptides were sequenced. The peptide sequences were compared with other PLs, oPRL and bGH for sequence similarity, and found to be most similar to bovine PL (bPL; 68% overall identity) and oPRL (47% overall identity). Complementary DNA (cDNA) clones were isolated for oPL by screening a λZAP cDNA library with a cDNA coding for bPL. Three cDNAs were nucleotide sequenced, and their combined sequence included 41 nucleotides of 5'-untranslated region, the complete coding region of pre-oPL (708 nucleotides) and a portion of the 3' untranslated region (158 nucleotides). The predicted amino acid sequence derived from the nucleotide sequence confirmed homology to bPL (67%) and oPRL (48%). Little amino acid sequence existed with other PLs (≤29%) or GH proteins (≤27%). These results suggest that oPL and oGH are more biologically similar in their ability to compete for fetal liver binding sites, but that oPL is structurally more similar to oPRL. Elucidation of exact structure–function relationships for oPL will, however, require further investigation.
Journal of Endocrinology (1990) 126, 141–149
Development of adenylate cyclase activity in rat adrenal glands during the perinatal period
Authors: Chatelain A. , Naaman E. , Durand P. , Lepretre A. , Dupouy J. P. 
Published: December 2008

ABSTRACT
Adenylate cyclase activity was studied in crude adrenal membranes from fetal and newborn rats. Basal adenylate cyclase activity was higher in fetal than in newborn rats. ACTH(1–24) (1 μmol/l), guanosine (β,γ-imido diphosphate) (Gpp(NH)p) (10 μmol/l) and forskolin (100 μmol/l) stimulated the activity of the enzyme at all stages studied. The sensitivity of the enzyme to ACTH was maximal on days 17 and 19 of gestation. When Gpp(NH)p was added to ACTH(1–24), the response was significantly higher than that induced by Gpp(NH)p alone. Forskolin and Gpp (NH)p alone increased the adenylate cyclase activity and the sensitivity of the enzyme to these compounds was higher in newborn rats than in fetuses. Treatment of 21-day-old rat fetuses with ACTH increased the response of adenylate cyclase to Gpp(NH)p alone or to forskolin whereas treatment with dexamethasone did not modify the response of the enzyme to either Gpp(NH)p alone or forskolin. Our results show that the change in the responsiveness of adenylate cyclase takes place immediately after birth during the first week and ACTH is able to induce a maturation of the fetal adrenal adenylate cyclase system.
Journal of Endocrinology (1990) 126, 211–216
Short-loop inhibition of thyrotrophin-releasing hormone-induced growth hormone secretion in fowl
Authors: Lea R. W. , Ahene C. A. , Marsh J. A. , Harvey S. 
Published: December 2008

ABSTRACT
The i.c.v. administration of 0·1 or 10 μg ovine (o)GH to 12- to 16-week-old hypothyroid chickens of a sex-linked dwarf (SLD) strain suppressed the basal plasma GH concentrations, measured 24 h afterwards. The GH response of the oGH-injected SLDs to TRH was suppressed, in a dose-related way, in comparison with that induced by TRH in birds given control injections (10 μg) of bovine serum albumin (BSA). Basal circulating concentrations of GH in euthyroid K strain birds of the same age were even lower than in the SLDs following injection of 10 μg oGH, and were not further reduced by oGH administration. The GH response to TRH in the K strain birds injected i.c.v. with 0·1 or 10 μg oGH was, nevertheless, suppressed in comparison with the BSA-injected K strain controls. The i.c.v. administration of oGH also suppressed circulating concentrations of LH and the LH response to TRH in the K strain birds.
Twenty-four hours after i.c.v. administration of oGH (10 μg), the somatostatin (SRIF) content in the medial basal hypothalamus of 8-week-old euthyroid cockerels was greater than that in BSA (10 μg)-injected controls. At the same time, the binding of [3H]3-methyl-histidine2-TRH to the pituitary caudal and cephalic lobes of GH-injected birds was less than that in the controls.
These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release.
Journal of Endocrinology (1990) 126, 237–244
Thyrotrophin increases the α1b-adrenergic receptors in rat thyroid gland in vivo
Authors: Shimura H. , Endo T. , Onaya T. 
Published: December 2008

ABSTRACT
Using chlorethylclonidine (CEC), an αlb-adrenergic receptor-selective antagonist, we characterized α1-adrenoceptor subtypes in rat thyroid gland, and investigated the effect of methimazole (MMI)-induced high TSH levels on α1 receptor subtypes and noradrenaline-induced iodide organification. The density of thyroid α1-adrenergic receptors was increased about sixfold in rats treated with MMI for 3 weeks compared with controls. Pretreatment of thyroid membrane preparations with CEC (10 μmol/l) caused an 83% decrease in specific 2-[β-(hydroxy-3-[125I]iodophenyl) ethylaminomethyl]tetralone binding sites in MMI-treated rats, but only a 43% decrease in control rats. The density of CEC-insensitive α1 receptors (α1a) was similar in MMI-treated and control rats, so MMI was shown to increase CEC-sensitive α1 receptors (α1b).
Noradrenaline-stimulated iodide organification was threefold greater in MMI-treated rats than in control rats when values were expressed as a per cent increase over basal levels. Pretreatment of thyroid lobes with 10 μmol CEC/1 for 30 min caused a 66% decrease in maximal noradrenaline-induced iodide organification in MMI-treated rats, but a significantly lower decrease (49%) in control rats.
These results suggest that the rat thyroid gland contains both α1a and α1b receptors, both of which mediate noradrenaline-induced iodide organification, and also that TSH enhances noradrenaline-induced iodide organification by increasing α1b receptor density.
Journal of Endocrinology (1990) 126, 317–322
Influence of oestrogen and progesterone on macrophage distribution in the mouse uterus
Authors: De M. , Wood G. W. 
Published: December 2008

ABSTRACT
Macrophages are constituents of all normal connective tissue including the murine uterus. Macrophages have been identified previously in endometrium and myometrium of pregnant and non-pregnant murine uterus using antibodies against macrophages. In the current study immunohistochemical analysis of murine uterus demonstrated that there were not significant quantitative differences in uterine macrophages between the dioestrous, pro-oestrous and oestrous stages. However, distributional changes occurred during the oestrous cycle. Macrophages were evenly distributed throughout uterine tissue during dioestrus, while, during pro-oestrus and oestrus, their concentration was highest in the subepithelial stroma. Because the oestrous cycle is hormonally regulated, we asked whether or not oestrogen and/or progesterone might influence macrophage distribution. Ovariectomy, which eliminates cyclical production of oestrogen and progesterone, resulted in a significant decrease in both the relative and the absolute number of uterine macrophages within 6 days. Injections of progesterone or oestrogen to ovariectomized mice resulted in restoration of uterine macrophage numbers. Injection of oestrogen plus progesterone in a regimen known to prepare the uterus for receptivity for blastocyst implantation increased the number of macrophages to levels which were consistently higher than those seen during oestrus. Moreover, following hormone administration macrophages were more concentrated in the subepithelial stroma, a distributional pattern which was most evident following injection of both hormones. The results suggest that both oestrogen and progesterone promote quantitative and distributional changes in the uterine macrophage population.
Journal of Endocrinology (1990) 126, 417–424
Increase in milk secretion and mammary blood flow by intra-arterial infusion of insulin-like growth factor-I into the mammary gland of the goat
Authors: Prosser C. G. , Fleet I. R. , Corps A. N. , Froesch E. R. , Heap R. B. 
Published: December 2008

ABSTRACT
The close-arterial infusion of free insulin-like growth factor-I (IGF-I; 1·1 nmol/min) for 6 h into the pudic artery supplying one mammary gland of lactating goats caused a 25±6% (mean ± s.e.m., n = 6) increase in the rate of milk secretion of that gland. The increase in the rate of milk secretion in the adjacent non-infused gland (14±4%) was not significantly different from that observed during saline infusion (4±5%). Blood flow to the infused gland was increased from 378±26 ml/min 1 h before to 487±56 ml/min approximately 5 h after the start of the infusion of IGF-I, declining to 420±44 ml/min approximately 2 h after the end of the infusion. The total concentration of IGF-I (free and bound) in milk of the infused gland was significantly higher than that of the non-infused gland. The concentrations of IGF-I in carotid arterial plasma samples increased during IGF-I infusion from a mean value of 32±2 nmol/l before to a maximum of 49±3 nmol/l 5 h after the infusion commenced. Circulating concentrations of total IGF-I declined slowly after the infusion with an estimated half-life of 5 h. Infusion of saline alone did not alter mammary blood flow or the concentration of total IGF-I in milk or plasma. The results indicate that the infusion of free IGF-I into the mammary arterial supply enhances milk secretion and mammary blood flow in intact, conscious goats. The more pronounced effect in the infused compared with the non-infused gland suggests that free IGF-I acts directly on the mammary gland. The response in the non-infused gland was attenuated presumably due to association of IGF-I with plasma binding proteins during recirculation.
Journal of Endocrinology (1990) 126, 437–443
Dexamethasone pretreatment of rat insulinoma cells decreases binding of glucagon-like peptide-1(7–36)amide
Authors: Richter G. , Göke R. , Göke B. , Arnold R. 
Published: December 2008

ABSTRACT
The effect of dexamethasone on binding of glucagonlike peptide-1(7–36)amide (GLP-1(7–36)amide) to rat insulinoma-derived cells (RINm5F) was investigated. Preincubation of RINm5F cells with dexamethasone (100 nmol/l) for 24 h resulted in a decrease of GLP1(7-36)amide binding to 55·0±8·16% (mean ± s.e.m.), incubation for 48 h to 39·1±1·76%, and for 72 h to 15·5±4·35% of maximal binding. The GLP-1(7–36)amide-induced stimulation of cyclic AMP (cAMP) production was significantly decreased to 61·03±7·4% of maximum production in cells pretreated with dexamethasone (100 nmol/l) for 48 h. The decreased binding was due to a reduction of the receptor number while the receptor affinity remained unchanged. These inhibitory effects on binding and cAMP formation induced by dexamethasone were completely abolished when the antiglucocorticoid RU 38486 (100 nmol/l) was added during preincubation with dexamethasone. RU 38486 alone had no effects. Our data suggest that the biological action of GLP-1(7–36) amide at the B-cell may be modified by glucocorticoids.
Journal of Endocrinology (1990) 126, 445–450
Insulin-like effect of vanadyl ion on streptozotocin-induced diabetic rats
Authors: Sakurai H. , Tsuchiya K. , Nukatsuka M. , Sofue M. , Kawada J. 
Published: December 2008

ABSTRACT
Recent studies have indicated that the blood glucose level of rats with streptozotocin (STZ)-induced diabetes (type 1) is normalized without an increase in the plasma insulin level by administration of sodium orthovanadate in the drinking water. The mechanism of this insulin-like effect of vanadate is unknown.
In this study, we investigated whether vanadyl ion, which is less toxic than vanadate to rats, also has an insulin-like effect in rats with STZ-induced diabetes. When rats with STZ-induced diabetes were given a daily i.p. injection of vanadyl sulphate (9·3 and 4·6 mg vanadium/kg body weight), their blood glucose level decreased from about 22·2 to about 7·2 mmol glucose/l within 2 days and remained low for at least 12 weeks. This treatment did not affect their low plasma insulin level. Quantitative electron spin resonance (ESR) spectrometry showed that most of the vanadium (about 90%) in their tissues was present as a vanadyl form (VO2+). ESR analysis also showed that the vanadyl ion in tissues was bound endogenously with four oxygen ligands from either water or oxyamino acid residues in proteins. Vanadyl sulphate accelerated glucose incorporation into adipocytes of rats, suggesting that the action of vanadyl ion is peripheral. Interestingly, vanadyl sulphate at a high concentration (about 10 mmol/l) was more effective than insulin in enhancing glucose uptake.
This study demonstrated that: (1) vanadyl sulphate (+ 4 oxidation state), like vanadate ion, normalizes the blood glucose levels of rats with STZ-induced diabetes; (2) the action of vanadyl ion is peripheral; and (3) the active form of vanadium for an insulin-like effect may be a vanadyl form, not vanadate.
Journal of Endocrinology (1990) 126, 451–459
Effects of trenbolone acetate and testosterone on growth and on plasma concentrations of corticosterone and ACTH in rats
Authors: Sillence M. N. , Rodway R. G. 
Published: December 2008

ABSTRACT
The effects of trenbolone acetate (TBA) on growth and on plasma concentrations of corticosterone were examined in male and female rats. At 5 weeks of age, rats were injected with TBA (0·8 mg/kg) dissolved in peanut oil, or with oil alone, daily for 10 days. In female rats, TBA caused an increase in weight gain (20–38%), a reduction in adrenal weight (19%) and a reduction in plasma concentrations of corticosterone (55%). In contrast, TBA-treated male rats showed no significant increase in weight gain, no significant change in adrenal weight and no reduction in plasma concentrations of corticosterone.
The mechanism by which adrenal activity was suppressed in TBA-treated female rats was examined and the response compared with that to testosterone. Female rats (8 weeks old) were injected daily either with oil vehicle, TBA (0·8 mg/kg) or testosterone propionate (0·8 mg/kg). Testosterone increased weight gain (24%), but the growth response to TBA treatment was significantly greater (97%). A reduction in plasma concentrations of corticosterone (45%) was again observed in response to TBA. However, testosterone increased plasma concentrations of corticosterone (52%) above those of control values. Neither androgen affected plasma concentrations of ACTH.
Finally, the effects of TBA were examined in 6-week-old female rats, to characterize further the apparent age-related increase in responsiveness. The growth response of 6-week-old rats (60–74%) was intermediate between that seen in 5- and 8-week-old animals.
It is concluded that part of the anabolic activity of TBA may be related to a reduction in circulating concentrations of corticosterone. The effect of TBA on corticosterone concentrations differs from that of the natural androgen, testosterone, and does not appear to be mediated by a reduction in plasma concentrations of ACTH.
Journal of Endocrinology (1990) 126, 461–466
Inhibin secretion during the ovulatory cycle and pregnancy in the common marmoset monkey
Authors: Smith K. B. , Lunn S. F. , Fraser H. M. 
Published: December 2008

ABSTRACT
Changes in plasma concentrations of immunoreactive inhibin in the reproductively cyclic, pregnant and ovariectomized female marmoset monkey (Callithrix jacchus) were measured with a heterologous radioimmunoassay. The pattern of inhibin secretion in five marmosets studied individually during four consecutive cycles was shown to resemble that of progesterone. In these animals, data were pooled according to stage of cycle on the basis of plasma progesterone concentrations. Mean values for inhibin were 5465 and 4972 U/l during the early and late follicular phase. Concentrations rose during the luteal phase to 8431, 12 246 and 12 557 U/l for the early, mid- and late luteal phase respectively. The hormonal profile of inhibin during the normal cycle is similar in both marmoset and stumptailed macaque; however, the marmoset has a 28-fold greater level of inhibin during the luteal phase.
In six marmosets in which pregnancy occurred, inhibin concentrations showed no decline at the end of the conceptual cycle and remained increased with respect to the follicular phase throughout the subsequent gestation. Inhibin levels were non-detectable (< 1000 U/l) in ovariectomized and acyclic marmosets.
These results suggest that the corpus luteum is the major source of inhibin in this New World monkey, in common with man and the Old World primates.
Journal of Endocrinology (1990) 126, 489–495
An insulin-like growth factor-binding protein purified from medium conditioned by a human lung fibroblast cell line (He[39]L) has a novel N-terminal sequence
Authors: Forbes B. , Ballard F. J. , Wallace J. C. 
Published: December 2008

ABSTRACT
We have identified a novel insulin-like growth factor (IGF)-binding protein secreted into the culture medium of a human lung fibroblast cell line (He[39]L). This binding protein was purified by S-Sepharose cation exchange chromatography, IGF affinity chromatography and reverse-phase high-performance liquid chromatography. Analysis of the He[39]L-binding protein on silver-stained polyacrylamide gels and by ligand blotting showed that it had a molecular weight of 32 kDa under non-reducing conditions. In charcoal competition binding assays, IGF-II competed at lower concentrations than IGF-I for binding to the He[39]L-binding protein and the more potent form of IGF-I (des-(1–3)-IGF-I) was not bound. This is a similar IGF binding pattern to that of the bovine IGF-binding protein-2 (bIGFBP-2). However, immunoblotting with an antibody to bIGFBP-2 demonstrated that the He[39]L-binding protein is not immunochemically related to bIGFBP-2. It is a glycosylated protein, having N-acetyl-glucosaminyl sugars detected by wheatgerm agglutinin affinity chromatography. Of the first 15 N-terminal amino acids of the He[39]L-binding protein, 13 are identical to the 15 amino acid sequence of a recently sequenced cerebrospinal fluid-binding protein. However, the total He[39]L-binding protein sequence (25 amino acids) showed no homology to other previously sequenced binding proteins (IGFBP-1, IGFBP-2 and IGFBP-3). We conclude that the He[39]L-binding protein is a novel binding protein.
Journal of Endocrinology (1990) 126, 497–506