Ontogeny and insulin-dependence of the satiation which follows carbohydrate absorption in the rat

Booth, D.A.; Jarman, S P

doi:10.1016/s0091-6773(75)91507-2

Cited by 50 publications

(6 citation statements)

References 16 publications

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“…The effects of intravenous infusions on food intake are probably no less sensitive to the physiological state of the animal. Absence of a detectable reduction of food intake during glucose infusion (Janowitz, Hanson & Grossman, 1949; Adair, Miller & Booth, 1968) has been attributed to insufficiency of insulin (Rowland, Meile & Nicolaidis, 1973;Booth & Jarman, 1975) or the distribution of glucose from an inappropriate infusion site (Russek, 1970;Campbell & Davis, 1974b). The rate of infusion can be too low (Strubbe, 1975) in relation to current absorption rate and the sensitivity of the satiety measurements (Pruvost, Duquesnel & Cabanac, 1973;Scharrer, Thomas & Mayer, 1974;VanderWeele, Novin, Rezek & Sanderson, 1974).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of food intake in the rat following complete absorption of glucose delivered into the stomach, intestine or liver.

Booth¹,

Jarman²

1976

The Journal of Physiology

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SUMMARY1. Solutions of glucose or other carbohydrates were administered during the dark or light period of the circadian cycle to rats which had been only briefly deprived of food.2. Food was restored to the animals at various times after administration of a glucose load by stomach tube. With delays between loading and access to food of up to 3 hr by night and 2 hr by day, subsequent food intake was less than intake after non-nutritive loads.3. Measurement of the glucose content of the gastrointestinal tract at various times after glucose loading showed that this depression of intake was still apparent even when the rat was offered food some time after complete absorption of the stomach load.4. Infusion of a glucose solution into the duodenum or the hepatic portal vein also inhibited subsequent food intake.5. In all cases, the inhibition of food intake was expressed as a decrease in the size of the first meal after restoring access to food.6. These results provide the first demonstration that the entry of normal amounts of carbohydrate into the body by the physiological route is followed by a depression of food intake which lasts until after absorption is complete.

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Section: Discussionmentioning

confidence: 99%

Inhibition of food intake in the rat following complete absorption of glucose delivered into the stomach, intestine or liver.

Booth¹,

Jarman²

1976

The Journal of Physiology

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“…That is not what is being proposed here. Instead, we imagine that satiety is normally associated with some consequence of the delivery of ade-quate utilizable calories and that insulin is important only to the extent that it influences metabolism and makes those calories utilizable (see also Booth & Jarman, 1975;Brobeck, 1975;Friedman, 1978;Nicolaidis & Rowland, 1976;VanderWeele, Pi-Sunyer, Novin, & Bush, 1980). Thus, satiety would not be expected in the postabsorptive state despite contrived hyperinsulinism (Rowland, Meile, & Nicolaidis, 1975;Strubbe et al, 1977;Thomas & Mayer, 1968), whereas it may occur in the absorptive state despite relative hypoinsulinism if the calories could nevertheless be utilized (Friedman, 1978).…”

Section: Discussionmentioning

confidence: 99%

“…During the past decade there has been a shift in attention from central mechanisms to peripheral factors that may be important in the control of feeding behavior (see reviews by Booth, 1978;Friedman & Strieker, 1976;Powley, 1977;Smith & Gibbs, 1979). From this perspective, satiety can be associated with the early postprandial state, when ingested metabolic fuels enter the circulation from the small intestine.…”

Section: Increased Feeding By Rats After Subdiabetogenic Streptozotoc...mentioning

confidence: 99%

Increased feeding by rats after subdiabetogenic streptozotocin treatment: A role for insulin in satiety.

Lindberg¹,

Coburn²,

Stricker³

1984

Behavioral Neuroscience

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Rats given streptozotocin showed varying degrees of glucose intolerance, ranging from mild to overt symptoms of diabetes mellitus. After being deprived of food overnight, both mild and overt diabetics consumed more food than controls did during 5-hr or 7-hr feeding tests. All animals ate large amounts of food during the first hour of the tests, but both groups of diabetics began to eat again sooner than controls did. Rats demonstrating the greatest degree of glucose intolerance before the test ate the most during the test. These and other findings suggest that feeding by diabetic rats after an overnight fast is an inverse function of their residual capacity for glucose utilization, which occurs despite elevations in blood glucose levels, and is not simply a compensatory response to glucose loss in urine. A modified glucostatic hypothesis is proposed in which insulin may normally promote satiety by influencing peripheral metabolism and making ingested calories utilizable.

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“…The role of the entero-insular axis in this prandial insulin release is well documented. It has been shown that inhibition of prandial insulin release by mannoheptulose suppresses satiation and accelerates the onset of subsequent feeding (Booth & Jarman 1975). Such a function of prandial hyperglycemia-hyperinsulinemia would explain why hepatic glucose production temporarily fails to control blood glucose constancy during meals.…”

Section: Slow Continuous Infusion I J Ui Ii M L I Hammentioning

confidence: 99%

“…The finding by Booth and Jarman (1975) that the inhibition of feeding persists beyond the complete intestinal absorption of a glucose load in the stomach Figure 11. Exhalation of M CO 2 ingested with a U C labelled food eaten at night extends to the subsequent day.…”

mentioning

confidence: 99%

Is food intake regulation based on signals arising in carbohydrate metabolism inherently inadequate for accurate regulation of energy balance on high-fat diets?

Flatt

1981

Behav Brain Sci

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Ontogeny and insulin-dependence of the satiation which follows carbohydrate absorption in the rat

Cited by 50 publications

References 16 publications

Inhibition of food intake in the rat following complete absorption of glucose delivered into the stomach, intestine or liver.

Inhibition of food intake in the rat following complete absorption of glucose delivered into the stomach, intestine or liver.

Increased feeding by rats after subdiabetogenic streptozotocin treatment: A role for insulin in satiety.

Is food intake regulation based on signals arising in carbohydrate metabolism inherently inadequate for accurate regulation of energy balance on high-fat diets?

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