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Tracy Josephs, Hayley Waugh, Ilona Kokay, David Grattan, and Mary Thompson

changes is still debated. Many other adipokines that have recently been identified in WAT have not been studied in relation to pregnancy and lactation. These other adipokines, which include fasting-induced adipose factor (FIAF), visfatin, apelin

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WS Zawalich and KC Zawalich

Islets from fed and 24-h-fasted rats were studied immediately after collagenase isolation. (1) After a 24-h fast, the insulin secretory responses to 8 mM glucose measured during perifusion were reduced by more than 90% from islets of fasted donors. (2) Increasing glucose to 11 or 27.5 mM resulted in enhanced insulin secretion from islets of fasted animals. (3) Fasting did not reduce islet insulin content. (4) Responses to 8 or 27.5 mM glucose were not affected if fatty acid-free albumin was used during the perifusion. (5) Inclusion of alpha-ketoisocaproate (5 mM), monomethyl succinate (10 mM) or carbachol (10 microM) significantly amplified insulin release from fasted islets in the simultaneous presence of 8 mM glucose. (6) Phospholipase C activation by glucose, carbachol or their combination was not adversely affected by fasting. (7) The response to the protein kinase C activator, phorbol 12-myristate 13-acetate (500 nM), was reduced by about 60% after fasting. (8) Extending the fast to 48 h resulted in a severe decline in response to 11 mM glucose; however, the further addition of 10 microM carbachol still enhanced release from these islets. The results confirm that caloric restriction impairs islet sensitivity to glucose stimulation and that protein kinase C may be involved in the reduction of glucose-induced insulin release from these islets. The activation of phospholipase C by cholinergic stimulation may contribute to the maintenance of insulin secretion from calorically restricted animals. These results also demonstrate that free fatty acids are not essential for glucose to evoke secretion from isolated islets of fasted donors.

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S. Harvey and H. Klandorf

The deprivation of food for 48 h markedly increased (P< 0·001) the corticosterone concentration in the plasma of 7- to 8-week-old chickens. When fasted birds were refed for 2 min or 5 s the corticosterone concentration fell to the level in fed birds within 30 min of refeeding. In fasted and refed birds the plasma corticosterone concentration remained lowered for at least 150 min after a 2-min period of refeeding, whereas in birds refed for 5 s the concentration had increased within 120 min to that in fasted birds. When fasted birds were refed 1, 5, 15 or 30 g diet the corticosterone level was again markedly reduced (P< 0·001) within 45 min of refeeding. The magnitude of this post-feeding decline was unrelated to the amount of food eaten, although its duration was; the level in birds refed 1, 5 or 15 g food increasing to that in fasted birds within 90, 135 and 225 min respectively. The corticosterone level in birds refed 30 g diet remained reduced for at least 225 min but increased to that in fasted birds 24 h after refeeding. The initial decline in the corticosterone concentration was unrelated to the consumption of food, since a similar reduction in the corticosterone level was observed in fasted birds which were given the sight of food but prevented from eating it by Perspex lids attached to the food troughs. This initial decline in the corticosterone level was not a result of stress, as it did not occur in fasted control birds. These results suggest that the adrenocortical changes in fasted and refed birds is initially mediated by a conditioned neural stimulus (reinforcement) and is maintained as a result of peripheral metabolic effects of ingested food.

In fasted chickens the concentration of plasma tri-iodothyronine (T3) was greatly reduced (P<0·001) in comparison with fed birds. When fasted birds were refed for 2 min or with 5, 15 or 30 g diet, the level of plasma T3 was increased (P < 0·05) 90 min after refeeding although not to the level in birds which had free access to food. The magnitude and duration of this increase was related to the amount of food consumed and was not observed in birds refed for 5 s or with 1 g food or in fasted birds given sight of but not access to food.

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R. G. Dyer, S. Mansfield, H. Corbet, and A. D. P. Dean


Two experiments were undertaken to investigate the way that fasting impairs LH secretion and to assess whether endogenous opioid mechanisms might be responsible for the impairment.

In the first experiment, pulsatile LH secretion was measured in a total of 51 chronically ovariectomized female rats. Initially 29 rats were subjected to food withdrawal for 24, 48, 72 or 120 h before the experiment. When compared with data collected from eight unfasted control rats, the 120-h fast was found to reduce significantly the mean peak and trough values of the LH pulses measured. However, in a subsequent study, the inhibition of pulsatile LH secretion by a 120-h fast was prevented in a group of eight rats given the opioid antagonist naloxone hydrochloride before the start of the blood-sampling period. Naloxone was without effect on pulsatile LH secretion in eight unfasted control rats.

In the second experiment, plasma LH concentrations were measured before and after unilateral electrical stimulation of the ventral noradrenergic tract (VNAT) in ovariectomized female rats pretreated with oestradiol benzoate. In 17 rats VNAT stimulation caused a significant rise in plasma LH, but after a 72-h fast this rise was significantly less than in unfasted control rats. However, pretreatment of fasted rats with naloxone (n = 9) significantly enhanced the VNAT-stimulated release of LH to the control values. Naloxone did not potentiate VNAT-stimulated LH release in unfasted animals (n = 6) or LH release in control unstimulated rats (n = 12).

The experiments indicate that both pulsatile LH secretion, and LH release caused by VNAT stimulation, are impaired by an acute fast. In both cases, the impairment is prevented by pretreatment with naloxone. Thus fasting probably activates an inhibitory opioid pathway within the brain to inhibit LH secretion.

J. Endocr. (1985) 105, 91–97

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Recently patients with refractory obesity have been treated by short periods of total deprivation of food (Bloom, 1959; Duncan, Jenson, Cristofori & Schless, 1963), and various metabolic changes following fasting have been studied (Cristofori & Duncan, 1964; van Riet, Schwarz & der Kinderen, 1964). We have reported elsewhere that the plasma level of inorganic iodine does not fall in euthyroid obese patients (Alexander, Harrison, Harden & Koutras, 1964), although during fasting there is evidence for decreased thyroid function (shown by a fall in the uptake of iodine by the thyroid gland and a fall in the level of serum protein-bound iodine). It was suggested that inorganic iodine concentration is maintained by the iodide derived from deiodination of thyroxine. It seemed possible that more direct evidence for this hypothesis could be obtained by studying the effect of fasting on the plasma inorganic iodide level in hypothyroid patients since less thyroxine would

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M. C. Neville, V. S. Sawicki, and W. W. Hay Jr


In order to determine whether short term variations in plasma glucose and/or insulin influence milk lactose secretion in women, the effects of fasting and increased blood insulin and glucose on milk volume and composition were studied with glucose clamp methodology in exclusively and partially breast-feeding women. Twenty hours of fasting had no discernable effect on the output of milk or its macronutrient composition. Four hours of increased plasma insulin, studied under conditions where plasma glucose was maintained at the fasting level, had no effect on milk volume, milk glucose concentration, total fat content or lactose secretion rate. Increased plasma glucose, maintained at twice fasting levels for 4 to 6 h, produced a threefold increase in milk glucose concentration but had no significant effect on the rate of lactose synthesis. In partially breast-feeding women producing no more than 200 ml milk per day, a similar degree of hyperglycaemia increased milk glucose more than fourfold but did not significantly increase the milk secretion rate. It is concluded that human milk production is isolated from the homeostatic mechanisms that regulate glucose metabolism in the rest of the body, in part because the lactose synthetase system has a K m for glucose lower than the concentration available in the Golgi compartment.

Journal of Endocrinology (1993) 139, 165–173

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Abnormal glucose tolerance is known to occur in the obese (Butterfield, Hanley & Whichelow, 1965) and Karam, Grodsky & Forsham (1963) have demonstrated increased insulin levels to be a feature of the response to a glucose load in overweight subjects. There has been no previous published work on the effects of prolonged starvation (over 14 days) on the carbohydrate metabolism of obese patients and this paper reports our findings in the first 12 subjects studied.

Twelve obese subjects (11F, 1M; aged 16–55 yr., 125–245% standard weight) were admitted to hospital and treated by complete starvation for 2½–18 weeks (mean 7). None were known to be diabetic. Before fasting an oral glucose tolerance test (50 g.) was performed and venous blood was removed for the determination of blood sugar, plasma insulin and free fatty acid (FFA) levels at 0, 30, 60, 90 and 120 min. The fast was terminated by administering

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M J Pesek and M A Sheridan


Somatostatins are a diverse family of peptides that influence various aspects of animal growth, development, and metabolism. Recent work in our laboratory has shown that somatostatins stimulate hepatic lipolysis in rainbow trout. In this study we characterized somatostatin-binding sites in trout hepatic membrane preparations. We also examined changes in binding characteristics brought about by food deprivation. Binding of [Tyr11]-somatostatin-14 (SS-14) was saturable, reversible, and time- and temperature-dependent. Under optimal conditions, [Tyr11]-SS-14 specific binding averaged 5·7 ± 0·3%. While SS-14 and SS-28 (an N-terminally extended form of SS-14 and derived from the same gene as SS-14) displaced [Tyr11]-SS-14 specific binding (ED50 values of approximately 50 nm and 100 nm respectively), salmon SS-25 (containing [Tyr7,Gly10]-SS-14 at its C terminus and presumably derived from a gene different from that giving rise to SS-14/SS-28), except at pharmacological concentrations, did not. Significant specific binding was also detected in brain, esophagus, stomach, upper and lower intestine, pancreas, and adipose tissue. Scatchard analysis suggested the existence of two classes of hepatic somatostatin-binding sites: a high-affinity site with a K d of 23 nm and Bmax of 1·4 pmol/mg protein and a low-affinity site with a K d of 379 nm and Bmax of 4·9 pmol/mg protein. Fasting resulted in reduced growth and elevated plasma levels of SS-14 compared with fed animals. SS-14 binding capacity of the high-affinity class in liver membranes isolated from fasted fish increased by 120% over that from fed counter-parts. No difference in K d for the high-affinity binding class or in either K d or Bmax of the low-affinity class was noted between fasted and fed animals. These data support the role of the liver as a target of somatostatin and suggest that fasting enhances hepatic sensitivity to SS-14 binding.

Journal of Endocrinology (1996) 150, 179–186

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The effects of injected glycine on the liver glycogen of fasting normal and adrenalectomized mice have been compared with those of injected glucose.

In both normal mice and cortisone-treated adrenalectomized mice glycine caused significant reduction in hepatic glycogen (Table 1).

In salt-maintained and in DOCA-treated adrenalectomized mice,glycine hada glycogen-sparing action, equivalent, carbon for carbon, to that of glucose.

These observations are related to the influence of C 11 oxygenated adrenal steroids on protein metabolism.

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Plasma insulin and growth hormone were measured by radioimmunoassay in healthy adults during the latter part of 22 hr. fasts and after graded glucose loads. The insulin concentration was less than 8 μ-u./ml. in all fasting samples and in samples taken after the blood glucose had returned to fasting levels. Insulin levels increased with increasing glucose loads.

During fasting, growth hormone showed intermittently raised secretion; in some subjects high values were reached at times which could not be related to external events or to stress. Growth hormone levels were consistently low during the absorption of glucose but rose immediately thereafter. This rise occurred increasingly late and reached increasing levels as the glucose loads were made progressively larger.

Insulin had almost invariably returned to fasting levels before the growth hormone concentrations began to rise.