Search Results

You are looking at 1 - 10 of 10 items for

  • Author: G. S. G. Spencer x
  • Refine by access: All content x
Clear All Modify Search
G. S. G. SPENCER
Search for other papers by G. S. G. SPENCER in
Google Scholar
PubMed
Close

Somatomedin activity, cortisol and free fatty acids have been measured in the plasma of eight Pietrain pigs at various times after stress. Somatomedin activity decreased immediately, reached a minimum after 15 min and remained low throughout a 3·5 h period. Cortisol levels rose to a peak after 15 min and regained normal levels after 60 min. Free fatty acid levels increased to a peak level about 3 h after stress.

The possibility of inhibitors of the bioassay for somatomedin activity influencing the results are discussed.

Restricted access
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close
and
G. M. Robinson
Search for other papers by G. M. Robinson in
Google Scholar
PubMed
Close

ABSTRACT

The effects of daily thyroxine (T4) administration to pregnant rats on the growth of their fetuses and placentae were examined. Additional trials examined the effect of such treatment on the postnatal growth of the offspring. Injection of 10 μg T4 into the mother caused a tenfold elevation in maternal plasma T4 concentration, which remained elevated for more than 12 h, but returned to basal levels by 24 h after injection. Despite the increase in maternal T4 concentrations, no increase in fetal plasma T4 was found. A greater weight of both the fetuses (20·1%; P<0·001) and placentae (14·6%; P<0·05) was found in the young of T4-treated mothers compared with those from control mothers at delivery by hysterotomy on day 20 of gestation. In trials where mothers delivered naturally, birth weights of the young from mothers treated with T4 (10, 20 or 50 μg daily) were also significantly heavier than controls, and continued to grow faster postnatally. These data suggest that maternal thyroid hormone status is important for fetal growth, and further indicate that stimulation of the thyroid hormone axis during pregnancy could provide a method for improving postnatal growth.

Journal of Endocrinology (1993) 139, 275–279

Restricted access
G. S. G. SPENCER
Search for other papers by G. S. G. SPENCER in
Google Scholar
PubMed
Close
and
A. M. TAYLOR
Search for other papers by A. M. TAYLOR in
Google Scholar
PubMed
Close

A simplified, more rapid bioassay for the estimation of somatomedin activity, based on the porcine costal cartilage bioassay, is described. A micro-scale system based on the porcine costal cartilage assay is also described. These assay systems showed no decrease in sensitivity or precision, compared with other methods, as a result of the modifications. The assays have been used for routine hospital laboratory determinations, for the estimation of somatomedin activity in normal adolescent children of both sexes and in clinical studies of scoliotic, acromegalic and hypopituitary patients.

Restricted access
G. M. Spencer
Search for other papers by G. M. Spencer in
Google Scholar
PubMed
Close
and
S. A. Whitehead
Search for other papers by S. A. Whitehead in
Google Scholar
PubMed
Close

ABSTRACT

The effects of the opiate antagonist naloxone on serum LH concentrations was investigated in gonadectomized rats given different regimes of steroid pretreatment. Two injections of testosterone given 48 and 24 h before naloxone treatment failed to reinstate LH responses to this drug in castrated rats while subcutaneous testosterone-filled silicone elastomer capsules implanted for a week were effective in this respect. Injections of oestrogen, oestrogen plus progesterone or progesterone alone all restored LH responses to naloxone in ovariectomized rats when given 48 and/or 24 h before drug treatment, although the magnitude of these responses varied according to the precise steroid treatments. The hypothalamic-pituitary axis was also responsive to naloxone just before the progesterone-induced LH surge in oestrogen-primed ovariectomized rats. Results show that gonadal steroids are permissive to the effects of opiate drugs, but they suggest that endogenous opioid systems do not necessarily mediate the negative feedback effects of steroids. Some other factor(s), as yet unidentified in the rat, may control the opioid modulation of gonadotrophin secretion or exert an independent inhibitory effect on gonadotrophin release.

J. Endocr. (1986) 110, 327–334

Restricted access
A. Cheung
Search for other papers by A. Cheung in
Google Scholar
PubMed
Close
,
S. Harvey
Search for other papers by S. Harvey in
Google Scholar
PubMed
Close
,
T. R. Hall
Search for other papers by T. R. Hall in
Google Scholar
PubMed
Close
,
S.-K. Lam
Search for other papers by S.-K. Lam in
Google Scholar
PubMed
Close
, and
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close

ABSTRACT

Young cockerels (6–8 weeks old) were injected with serum from sheep immunized against somatostatin-14 (anti-SRIF) or normal sheep serum (NSS). Blood samples were withdrawn periodically for the determination of plasma corticosterone concentration by radioimmunoassay. With frequent (every 10 min) sampling, NSS-treated control animals exhibited increased plasma corticosterone levels, presumably as a stress response to the experimental manipulation. Anti-SRIF stimulated a much greater increase in plasma corticosterone concentrations and a peak response was observed within 10 to 20 min, when the plasma corticosterone level reached more than twice that of the corresponding control value. With less frequent sampling, plasma corticosterone increased with anti-SRIF administration to as much as nine times the corresponding control value, and the peak response occurred much later. Under pentobarbitone anaesthesia, which itself increased basal corticosterone concentrations, anti-SRIF treatment promoted further increases in plasma corticosterone levels although to a smaller magnitude compared with conscious birds. The results suggest that endogenous somatostatin may play a role in the regulation of adrenocortical function in the domestic fowl. The mechanism of response may involve a central component.

J. Endocr. (1988) 116, 179–183

Restricted access
S.-K. Lam
Search for other papers by S.-K. Lam in
Google Scholar
PubMed
Close
,
S. Harvey
Search for other papers by S. Harvey in
Google Scholar
PubMed
Close
,
T. R. Hall
Search for other papers by T. R. Hall in
Google Scholar
PubMed
Close
, and
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close

ABSTRACT

The influence of somatostatin on thyroid function has been examined in immature domestic fowl passively immunized with somatostatin antiserum. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations were markedly increased within 10 min of antisomatostatin administration and remained raised for at least 5 h. The increases in the T3 and T4 concentrations following somatostatin immunoneutralization were directly related to the volume of antisera administered. The increase in the T3 concentration exceeded the increase in the T4 concentration, resulting in a T3: T4 ratio greater than unity. While the raised T4 concentration began to decline 30 min after antisomatostatin administration, raised T3 concentrations were sustained for at least 2 h, and further increased the plasma T3: T4 ratio.

These results demonstrate that somatostatin immunoneutralization stimulates thyroid function in fowl. The magnitude and rapidity of the thyroidal responses to somatostatin immunoneutralization suggests that they occur independently of the hypothalamic-pituitary-thyroid axis. Somatostatin appears to exert a tonic inhibitory control on avian thyroid function, possibly by effects mediated at the thyroid gland to inhibit T4 release and by peripheral effects to suppress the conversion of T4 and T3.

J. Endocr. (1986) 110, 127–132

Restricted access
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close
,
G. J. Garssen
Search for other papers by G. J. Garssen in
Google Scholar
PubMed
Close
,
B. Colenbrander
Search for other papers by B. Colenbrander in
Google Scholar
PubMed
Close
, and
J. C. Meijer
Search for other papers by J. C. Meijer in
Google Scholar
PubMed
Close

ABSTRACT

The effects of i.v. administration of thyrotrophin-releasing hormone (TRH) and of somatostatin on circulating plasma levels of porcine GH in the chronically catheterized pig fetus have been examined. Growth hormone levels increased markedly (P<0·01) following TRH administration, but there was no change in thyroxine levels by 1 h after treatment. Administration of somatostatin caused a significant (P<0·05) decrease in mean GH levels, but the response was variable between pigs. Saline administration had no significant effect on GH levels. These results suggest that the mechanisms regulating postnatal GH release are present in the fetal pig, but may not be fully developed 8–12 days before delivery.

J. Endocr. (1985) 106, 121–124

Restricted access
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close
,
D. J. Hill
Search for other papers by D. J. Hill in
Google Scholar
PubMed
Close
,
G. J. Garssen
Search for other papers by G. J. Garssen in
Google Scholar
PubMed
Close
,
A. A. Macdonald
Search for other papers by A. A. Macdonald in
Google Scholar
PubMed
Close
, and
B. Colenbrander
Search for other papers by B. Colenbrander in
Google Scholar
PubMed
Close

Chronic hyperinsulinaemia in the presence of euglycaemia was obtained in pig fetuses between 90 and 104 days gestational age (term is 114 days) by the implantation of insulin-filled osmotic minipumps. At 104 days these fetuses were compared with both saline-implanted controls and with unoperated fetuses from the same sows.

Mean plasma GH levels were the same in all three treatment groups and were much greater than in the maternal peripheral venous circulation. Levels of GH in amniotic fluid were low, and even lower levels were measured in lung fluid. Glucose and protein levels were also lower in amniotic fluid than in plasma and lower still in lung fluid. In contrast, somatomedin activity was higher in amniotic and lung fluids than in fetal plasma and, when expressed relative to protein content, was highest in lung fluid. Insulin-treated fetuses had significantly (P < 0·05) higher levels of somatomedin activity than control fetuses, but despite this were neither longer nor heavier than control fetuses. From these data it is concluded that neither insulin nor somatomedin directly affect fetal growth.

Restricted access
K. M. Hua
Search for other papers by K. M. Hua in
Google Scholar
PubMed
Close
,
R. Ord
Search for other papers by R. Ord in
Google Scholar
PubMed
Close
,
S. Kirk
Search for other papers by S. Kirk in
Google Scholar
PubMed
Close
,
Q. J. Li
Search for other papers by Q. J. Li in
Google Scholar
PubMed
Close
,
S. C. Hodgkinson
Search for other papers by S. C. Hodgkinson in
Google Scholar
PubMed
Close
,
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close
,
P. C. Molan
Search for other papers by P. C. Molan in
Google Scholar
PubMed
Close
, and
J. J. Bass
Search for other papers by J. J. Bass in
Google Scholar
PubMed
Close

ABSTRACT

Tissue and plasma levels of insulin-like growth factor-I (IGF-I), and relative levels of liver IGF-I RNA, were measured in 6-month-old ewe lambs which were well fed (n = 10) or starved (n = 10) for 5 days. Half of each nutrition group was given daily (09.00 h) injections of human GH (hGH; 0·15 mg/kg body weight per day). Blood was sampled daily from 09.00 to 12.00 h at 15-min intervals through jugular vein catheters and the lambs were slaughtered 24 h after the fifth injection of hGH.

Tissue and plasma IGF-I was extracted using an acid-ethanol-cryo-precipitation technique and estimated by radioimmunoassay. Tissue IGF-I was corrected for retained plasma IGF-I using tissue and blood haemaglobin levels. Liver IGF-I RNA levels were monitored by in-situ hybridization.

Plasma IGF-I (nmol/l) was higher in both the fed group and the fed group given GH treatment. Tissue IGF-I from kidneys (nmol/kg) was also higher (P < 0·001) in the fed group. There was no significant difference in IGF-I concentrations in the muscle biceps femoris or liver between fed and starved lambs. Although GH treatment did not increase IGF-I levels in tissues significantly, IGF-I RNA levels in liver were increased (P = 0·02) in both fed and starved animals. The relative liver IGF-I RNA levels positively correlated with their corresponding tissue IGF-I levels in the fed group and the fed group given GH treatment. The lack of a significant IGF-I response to GH in tissues may be due to either the time at which tissues were sampled after the GH treatment or the dose of GH administered. However, the higher IGF-I concentrations in plasma and kidney from fed compared with starved animals and the positive correlations between liver IGF-I and IGF-I RNA levels suggest that tissue and plasma IGF-I is regulated by nutrition and GH, with nutrition playing a critical role in the regulation of tissue and plasma IGF-I in normal lambs.

Journal of Endocrinology (1993) 136, 217–224

Restricted access
J. L. Elliott
Search for other papers by J. L. Elliott in
Google Scholar
PubMed
Close
,
J. M. Oldham
Search for other papers by J. M. Oldham in
Google Scholar
PubMed
Close
,
G. R. Ambler
Search for other papers by G. R. Ambler in
Google Scholar
PubMed
Close
,
P. C. Molan
Search for other papers by P. C. Molan in
Google Scholar
PubMed
Close
,
G. S. G. Spencer
Search for other papers by G. S. G. Spencer in
Google Scholar
PubMed
Close
,
S. C. Hodgkinson
Search for other papers by S. C. Hodgkinson in
Google Scholar
PubMed
Close
,
B. H. Breier
Search for other papers by B. H. Breier in
Google Scholar
PubMed
Close
,
P. D. Gluckman
Search for other papers by P. D. Gluckman in
Google Scholar
PubMed
Close
,
J. M. Suttie
Search for other papers by J. M. Suttie in
Google Scholar
PubMed
Close
, and
J. J. Bass
Search for other papers by J. J. Bass in
Google Scholar
PubMed
Close

ABSTRACT

Insulin-like growth factor-II (IGF-II) binding in the growing tip of the deer antler was examined using autoradiographical studies, radioreceptor assays and affinity cross-linking studies. Antler tips from red deer stags were removed 60 days after the commencement of growth, and cryogenically cut into sections. Sections were incubated with radiolabelled IGF-II, with or without an excess of competing unlabelled IGF-II and analysed autoradiographically. Radiolabelled IGF-II showed high specific binding in the reserve mesenchyme and perichondrium zones, which are tissues undergoing rapid differentiation and cell division in the antler. Binding to all other structural zones was low and significantly (P<0·001) less than binding to the reserve mesenchyme/perichondrium zones. Radioreceptor assays on antler microsomal membrane preparations revealed that the IGF-II binding was to a relatively homogeneous receptor population (K d= 1·3 × 10−10 mol/l) with characteristics that were not entirely consistent with those normally attributed to the type 2 IGF receptor. Tracer binding was partly displaceable by IGF-I and insulin at concentrations above 10 nmol/l. However, affinity cross-linking studies revealed a single band migrating at 220 kDa under non-reducing conditions, indicative of the type 2 IGF receptor. These results indicate that, in antler tip tissues, IGF-II binds to sites which have different binding patterns and properties from receptors binding IGF-I. This may have functional significance as it appears that, whilst IGF-I has a role in matrix development of cartilage, IGF-II may have a role in the most rapidly differentiating and proliferating tissues of the antler.

Journal of Endocrinology (1993) 138, 233–241

Restricted access