Anterior pituitary extracts and liver fat1

Best, C. H.; Campbell, James E.

doi:10.1113/jphysiol.1936.sp003354

Cited by 94 publications

(7 citation statements)

References 3 publications

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“…Production of fatty livers by fasting in mammalian species was established several decades ago. Best and Campbell (1936) observed a range of liver fat from 5.3 to 6% in rats fasted for 3 days compared to a range of 3.8 to 4.5% in fed rats. In a study with mice, Barrett et al (1936) observed an increase in liver fat from three to five times that observed in fed animals when the mice were fasted for 2 to 7 days.…”

Section: Introductionmentioning

confidence: 80%

Liver Lipid Content in Broilers as Affected by Time Without Feed or Feed and Water

1984

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The purpose of this study was to determine if length of time of feed withdrawal of broilers prior to slaughter could affect the lipid content of their livers. Seven-week-old male broilers were allocated to three treatments: 1) no feed and water, 2) no feed, and 3) feed and water ad libitum. Those in the first treatment were held in plastic coops and those in the latter two treatments were kept in floor pens. Eight birds were randomly sampled initially and eight birds from each treatment at 4, 8, 12, 16, and 24 hr after the start of the study. The birds were weighed, killed, and the livers removed and analyzed for lipid content. The regression slopes of the two treatments without feed for body weight, liver weight, liver weight per unit body weight, and liver fat per unit body weight were significantly different from the control treatment. The slopes for liver fat were not significantly different among treatments. No obvious differences in the gross appearance of the livers were detected. The occasional problems with fatty livers in commercial broilers apparently cannot be accounted for by the length of time of feed withdrawal before slaughter.

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Section: Introductionmentioning

confidence: 80%

Liver Lipid Content in Broilers as Affected by Time Without Feed or Feed and Water

1984

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“…This process is in part under the control of the anterior pituitary. Best and Campbell ( 1936) prepared an extract from the anterior pituitary which, when injected into rats, causcd ketoncmia and increased the size and fat content of the liver. Using similar chemical procedures, Weil and Stetten (1947) prepared an extract from the urine of fasting rabbits which, like that from the anterior pituitary, caused an increase in liver fat of the mouse.…”

Section: Discussionmentioning

confidence: 99%

A fat-mobilizing substance in chicken urine

Nir¹,

Dimick²,

Lepkovsky³

1969

Can. J. Physiol. Pharmacol.

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NIR, I.. DIMICK, M. K., AND LEPKOVSKY, S. 1969. A fat-mobilizing substance in chicken urine. Can. 5. Physiol. Pharrnacol. 47,[435][436][437][438][439][440][441][442][443].A fat-mobilizing substance (FMS) was cxtracted from the urine of fasting male and female chickens. Injection into chickens caused transient decreases in food intake and transient increases in plasma free fatty acids (FFA). These eEecls were accompanied by persisting decreases in plasma triglycerides. FMS also caused persistent decreases in plasma choBestero1 and Iipid phosphorus. Slight elevations of blood gltacose occurred, but they were: not statistically significant. FMS obtained from the urine of fed chickens by the same technique as that based with fasting chickens varied in its activity; at times it was similar to the FMS obtained from fasting chickens and at other times had little effect on plasnla FFA and food intake. FMS elicited snlaller increases in plasma FFA in laying hens than it did in males, possibly as a resujt of higher prc-injection levels in the hens. In contrast to findings in mammals, FMS was obtained from the urine of hypophysectomized chickens. DifTesences in response to FMS among mice, rats, and chickens are discussed.

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“…Various physiological and pathological conditions are associated with elevated concentrations of ketone bodies and growth hormone such as exercise [1], poor metabolic control [2], ketoacidosis [3] and post-hypoglycaemia ketosis [4] in diabetic subjects, and alcoholic ketoacidosis [5]. Administration of pharmacological amounts of growth hormone induced ketosis in animals [6][7][8]. Several studies in man demonstrated lipolytic and ketogenic effects of pharmacological doses of growth hormone [9][10][11].…”

Section: Key-wordsmentioning

confidence: 99%

Effect of physiological elevation of plasma growth hormone levels on ketone body kinetics and lipolysis in normal and acutely insulin-deficient man

et al. 1984

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Summary. The effect of physiological elevation of growth hormone levels on ketone body kinetics was determined using a 14C-ketone body tracer technique in normal and acutely insulin-deficient man. Changes of ketone body production and metabolic clearance rates during growth hormone infusion (plasma levels of approximately 25 ~tg/1) were measured during basal conditions and during heparin-induced elevation of non-esterified fatty acid levels. Growth hormone administration to six subjects fasted overnight resulted in an increase in ketone body production which exceeded that observed in nine control subjects (5.5 _+ 0.5 versus 3.1 _+ 0.1 ~tmol. kg q-min 4, p < 0.025) after elevation of plasma non-esterified fatty acids. Growth hormone infusion increased glycerol and non-esterified fatty acid concentrations indicating enhanced lipolysis. During somatostatin-induced acute insulin deficiency (n = 7), growth hormone enhanced the increase in total ketone body production observed in six subjects receiving somatostatin alone (8.4+0.8 versus 4.1_+0.7 txmol.kg -1.rain q, p<0.01). Total ketone body metabolic clearance decreased by 50% during somatostatin and remained uninfluenced by growth hormone. Non-esterified fatty acids and glycerol levels increased during somatostatin, and growth hormone failed to alter nonesterified fatty acid levels significantly. The results demonstrate a stimulatory effect of high physiological growth hormone levels on ketogenesis which is largely explained by an enhancement of lipolysis and thus increase in substrate supply for ketogenesis. Growth hormone administration during acute insulin deficiency enhanced ketogenesis in the absence of alterations in plasma non-esterified fatty acid levels, suggesting a direct hepatic ketogenic effect.

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Anterior pituitary extracts and liver fat1

Cited by 94 publications

References 3 publications

Liver Lipid Content in Broilers as Affected by Time Without Feed or Feed and Water

Liver Lipid Content in Broilers as Affected by Time Without Feed or Feed and Water

A fat-mobilizing substance in chicken urine

Effect of physiological elevation of plasma growth hormone levels on ketone body kinetics and lipolysis in normal and acutely insulin-deficient man

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