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ABSTRACT

The participation of the ovarian steroids and opioid peptides in the suppression of pulsatile LH release during acute fasting was examined in rats. Ovariectomized rats bearing silicone elastomer implants of oestradiol and/or progesterone were fasted for 48 h and subsequently blood samples were taken every 6 min for 3 h. Pulsatile LH release was suppressed after 48 h of fasting in the ovariectomized rats implanted with oestradiol but not in the oil-implanted controls. This suppression was enhanced after the administration of progesterone together with oestradiol.

In a second experiment, ovariectomized rats bearing implants of oestradiol or oil were fasted for 48 h and injected s.c. (2·5 mg/kg body weight) with an opioid antagonist, naloxone hydrochloride, immediately before blood sampling. In the fasted oestradiol-treated ovariectomized rats, naloxone was able to prevent the suppression of pulsatile LH release. In the absence of oestradiol, however, naloxone was without effect on LH release in either the fasted or unfasted animals.

These experiments indicate that the suppression of pulsatile LH release after 48 h of fasting is dependent upon oestradiol and that endogenous opioids are involved in the suppression.

Journal of Endocrinology (1991) 129, 321–328

SUMMARY

1. In fasted adrenalectomized female rats a rise in blood sugar may be a more sensitive index of cortisone activity than a rise in liver glycogen.

2. There was a threshold level of blood sugar below which the liver was almost empty of glycogen. Above this threshold the concentration of liver glycogen rose almost logarithmically with a rise in blood sugar.

3. The shape of this blood sugar—liver glycogen relationship is discussed in relation to the bio-assay of corticosteroids and their effect on carbohydrate metabolism.

4. The concentration of glucose in the red cell of the rat is much less than that in the plasma.

ABSTRACT

Circadian fluctuations of plasma calcium and immunoassayable calcitonin levels were studied in normal and calcium-deficient 2-month-old rats. The relationship between these parameters was also studied in animals which had been fasted for short periods. The plasma calcium rhythm persisted and was even amplified in rats placed on a 4-week calcium-deficient diet. In these rats, as in normal rats, the plasma calcium concentration diminished during the dark period. Calcitonin levels increased at the onset of the feeding period in normal rats but, in calcium-deficient rats, the pattern changed completely, with a major peak at the end of the light period and remaining at a low level during the dark feeding period. This modification of calcitonin rhythmicity appeared to be dependent on the degree of calcium deficiency. Fasting had little effect on calcitonin rhythms in either normal or calcium-deficient rats.

It is concluded that the calcitonin rhythm is relatively independent of feeding per se and that there appears to be no simple relationship between plasma calcium and calcitonin concentrations. It is suggested that the results may best be interpreted as reflecting the presence of rhythmic endogenous phenomena which are intrinsic to calcium metabolism and its regulation in the rat.

J. Endocr. (1985) 107, 389–395

ABSTRACT

We have examined the relationship between the changes in resting metabolic rate (RMR) and those in hepatic metabolism induced by hyperthyroidism and fasting for 24 h. We found that hyperthyroidism induced a significant increase in RMR, while fasting for 24 h reduced RMR in euthyroid but not in hyperthyroid rats. We have also measured oxygen consumption in isolated hepatocytes from euthyroid and hyperthyroid rats, fed or fasted for 24 h. Hyperthyroidism induced an increase in oxygen consumption in rat liver cells; fasting for 24 h increased respiratory rates in isolated liver cells from euthyroid but not from hyperthyroid rats.

The findings showed that hyperthyroidism and fasting for 24 h have opposite effects on RMR but similar effects on hepatic metabolism. The results also indicated that the increase in RMR found in hyperthyroid rats is partly due to an increase in hepatic metabolism, while no correlation exists between variations in resting and hepatic metabolism induced by 24-h fasting.

Journal of Endocrinology (1992) 135, 45–51

Circulating levels of somatomedins in man and rats are reduced by fasting and restored by refeeding. To determine the mechanisms for these alterations in somatomedin levels, the affinities and binding capacities of ¹²⁵I-labelled bovine GH (somatogenic binding sites) and of ¹²⁵I-labelled ovine prolactin (lactogenic binding sites) were assessed in liver homogenates from fasted and refed rats. Correlations were made with plasma immunoreactive somatomedin-C (Sm-C) and plasma insulin.

During fasting and refeeding there was a close temporal relationship between the fall and the rise of plasma levels of Sm-C and insulin, and the number of hepatic GH binding sites. After fasting for 1 day, plasma Sm-C dropped by 68% and plasma insulin by 76% when compared with values before fasting. At the same time, GH binding capacity was significantly reduced (7·3 ± 2·8 (s.e.m.) pmol/liver v. controls, 20·3 ± 2·1 pmol/liver; P < 0·01). Refeeding for 24 h normalized plasma insulin levels and restored GH binding capacity to values before fasting (13·2 ± 2·4 v. 20·3 ± 2·1 pmol/liver; P > 0·05). Plasma Sm-C rose significantly with refeeding and returned to initial values at day 4 of refeeding (0·82 ± 0·10 v. 0·77 ± 0·07 units/ml; P > 0·05).

In contrast, changes in prolactin binding sites correlated poorly with changes in plasma Sm-C. There was a modest decline with fasting significant only after 72 h (6·8 ± 0·6 v. 13·9 ± 3·2 pmol/liver; P < 0·05), and refeeding for 24 h did not restore prolactin binding (5·7 ± 1·2 pmol/liver).

Since a number of reports suggest that fasting induces a state of tissue insensitivity to GH, our findings suggest that the reduction in hepatic GH binding capacity might be a mechanism for the fasting-induced reduction in Sm-C. The reduction in plasma insulin, which accompanies fasting, might play a permissive role in the intracellular metabolic events involved in Sm-C and GH receptor regulation.

ABSTRACT

The Pharmacia fast protein liquid chromatography system was employed to fractionate a purified preparation of human LH (hLH) on the anion exchanger Mono Q at pH 7·8 into 14 sub-fractions. Each of the sub-fractions was characterized by its behaviour on polyacrylamide gel electrophoresis, sodium dodecyl sulphate (SDS) gel electrophoresis, LH receptor binding activity and sialic acid content. All sub-fractions contained sialic acid, were active in binding to LH receptors, and exhibited components typical of hLH subunits on SDS gel electrophoresis. None of the sub-fractions was homogeneous with respect to charge. There is evidence that part of the heterogeneity results from the presence in some molecules of an internal proteolytic cleavage within the β-subunit, and fractions enriched in species containing such cleavages were prepared by this method.

J. Endocr. (1985) 105,405–413

Hyperglycaemia was produced in chronically catheterized fetal lambs and pregnant ewes by the infusion of glucose into the fetus. Plasma concentrations of placental lactogen did not change significantly in either fetal or maternal circulations. Fetal and maternal hypoglycaemia was induced by administration of insulin to the fetus and ewe separately. Plasma concentrations of placental lactogen in the fetus did not change significantly but maternal plasma concentrations fell slightly after hypoglycaemia in either fetus or ewe. Plasma concentrations of placental lactogen rose in both the ewe and fetus during prolonged fasting of the ewe. These results neither confirm nor refute a role for placental lactogen in intermediary metabolism of the pregnant ewe and fetus but glucose concentration alone is unlikely to be a significant factor in the control of secretion of this hormone.

ABSTRACT

White Leghorn male chicks of 40 days of age were fasted for 5 days and then refed. Blood samples were collected from these chicks before, during and after fasting and serum levels of GH and insulin-like growth factor-I (IGF-I) and serum IGF-I-binding activity were determined. The fasting-induced reduction in body weight was accompanied by a significant rise in circulating GH and fall in IGF-I, coupled with increased serum IGF-I-binding activity. When pooled serum was chromatographed under neutral conditions, IGF-I binding activity and IGF-I immunoreactivity were mainly associated with a large (M _r= 150 000) and a small protein (M _r=30 000). Fasting induced a marked increase in the IGF-I-binding activity of the 30 kDa IGF-I-binding protein (IGFBP) and refeeding restored activity to the normal levels seen before fasting. Ligand blotting of serumbinding proteins with ¹²⁵I-labelled IGF-I, after first subjecting the samples to polyacrylamide gel electrophoresis and transfer to nitrocellulose, revealed that four IGFBPs (M _r=20 000, 30 000, 35 900 and 41 000) were present in chicken serum, and that the ¹²⁵I-labelled IGF-I binding of the 30 kDa monomer was increased by fasting and restored to normal by refeeding in agreement with gel filtration profiles of IGF-Ibinding activity. Western blot analysis suggested that the 30 kDa IGFBP is homologous to IGFBP-2 found in mammalian blood plasma. The results show that IGFBPs in chicken serum and their responses to fasting are similar to those in mammals.

Journal of Endocrinology (1993) 139, 363–370