Hepatic Receptors and the Neurophysiological Mechanisms Controlling Feeding Behavior

Russek, M.

doi:10.1016/b978-0-12-512504-8.50012-3

Cited by 80 publications

(33 citation statements)

References 136 publications

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“…In view of the short latency of anorectic activity it is possible that there are peripheral sites of action, particularly since labelled linoleic acid has been shown to accumulate in liver and adipose tissue (Panksepp, 1975), areas which have been shown to contain receptors that participate in the regulation of the hunger-satiety phenomenon (Russek, 1971). Evidence for a prostaglandin generating system at the hypothalamic level is that the precursor fatty acids cross the blood brain barrier (Alfin-Slater & Aftergood, 1968) and that hypothalamic centres concerned with regulation of food intake have been demonstrated to accumulate labelled linoleic acid when given intragastrically (Panksepp, 1975).…”

Section: Resultsmentioning

confidence: 99%

Anorectic Activity of Prostaglandin Precursors

Doggett

Jawaharlal

1977

British J Pharmacology

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1 Intraperitoneal and intragastric (i.g.) administration of prostaglandin precursors arachidonic (2 mg, 15 mg/kg, i.p.; 30 mg/kg, i.g.), linolenic (100 mg/kg, i.p.; 200 mg/kg, i.g.) and linoleic (15, 100 mg/kg, i.p.; 100 mg/kg, i.g.) acids to 22 h food‐deprived rats inhibits food intake. 2 This anorexia is similar to that induced by prostaglandin F2α (1 mg/kg, i.p.). 3 At anorectic doses these fatty acids do not cause pyrexia, in fact arachidonic acid causes hypothermia. 4 Prior treatment with indomethacin (15 mg/kg) and paracetamol (50 mg/kg) specifically reverses the anorexia and the behavioural satiety induced by the three fatty acids, while not affecting prostaglandin F2α‐induced suppression of food intake. 5 Results of the present experiments suggest that both physiological and pharmacological modification of appetite could be brought about through an effect on prostaglandin generating systems.

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Section: Resultsmentioning

confidence: 99%

Anorectic Activity of Prostaglandin Precursors

Doggett

Jawaharlal

1977

British J Pharmacology

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“…First, Mayer (3) suggested that glucose-sensitive neurons located in specific areas of the central nervous system exert positive or negative feedback on food intake (the glucostatic theory). Later, Russek (4) argued that glucose receptors are present in the liver (the hepatostatic hypothesis) and therefore that liver glycogen content influences food intake. More recently, Flatt (5) proposed that carbohydrate status could play an important role in the regulation of food intake (the glycogenostatic model) because of the priority given by the body to the carbohydrate balance over the fat balance.…”

Section: Introductionmentioning

confidence: 99%

Substrate oxidation influences liking, wanting, macronutrient selection, and consumption of food in humans

Brondel¹,

Landais²,

Romer³

et al. 2011

The American Journal of Clinical Nutrition

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Background: Several carbohydrate-based models of feeding have been described. The influence of the substrate oxidation rate on liking, wanting, and macronutrient selection, however, is not known in humans. Objective: The aim of this study was to investigate the influence of the substrate oxidation rate on the above variables. Design: A randomized 4-condition study was conducted in 16 normalweight men (mean 6 SD age: 23 6 3 y). The sessions differed in the composition of breakfast, which was either high in carbohydrates (HC) or low in carbohydrates (LC) or high in fat (HF) or low in fat (LF). Two hours and 20 minutes after breakfast, energy expenditure (EE) and respiratory exchange ratios (RERs) were measured. Next, olfactory liking for 4 foods (sweet and fatty) and ad libitum energy intake (carbohydrate-and fat-rich bread) were evaluated. Results: EE was higher (P , 0.001) and subsequent intake was lower (P , 0.01) after the HC and HF breakfasts than after the LC and LF breakfasts. The HC and LC breakfasts induced a higher RER (P , 0.001), lower olfactory liking for sweet foods (P , 0.05), and the consumption of a lower proportion of carbohydrate-rich bread (P, 0.05) than did the HF and LF breakfasts. The HF breakfast induced the lowest RER (P , 0.001), the lowest olfactory liking for fatty foods (P , 0.05), and the lowest proportion of fat-rich bread consumed (P , 0.01). Above all, a negative correlation was found between the RER and olfactory liking for sweet foods (P , 0.001). Conclusion: A high fat oxidation rate induces a strong liking for carbohydrates and a low liking for fats, which lends new support to the carbohydrate-based model of feeding. This trial is registered at clinicaltrials.gov as NCT01122082.Am J Clin Nutr 2011;94: 775-83.

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“…Since an adipokinetic mechanism has been demonstrated (Panksepp & Pilcher, 1973) within the hypothalamus it is most likely that prostaglandins might be released there and act as local transmitters. Since the liver contains receptors for regulation of food intake (Russek, 1971) and since prostaglandins are accumulated in large quantities (Bergstrom, Carlson & Weeks, 1968) in this organ, this might be their other site of action.…”

Section: Discussionmentioning

confidence: 99%

SOME OBSERVATIONS ON THE ANORECTIC ACTIVITY OF PROSTAGLANDIN F_2α

Doggett¹,

Jawaharlal²

1977

British J Pharmacology

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I Intracerebroventricular injection of prostanglandin F2a (10-40 jg) decreases food intake in a dosedependent manner in rats trained to consume their daily total food intake in a 2 h period. 2 This anorexia is also observed in satiated rats, which had ad libitum access to food. 3 The anorectic activity of prostaglandin F2a is not modified by changes in the internal environment of the body after food intake, such as increased blood glucose and insulin levels and decreased fatty acid levels, or by the presence or absence of food in the stomach, as is evident from the anorectic activity of prostaglandin F2a in partially satiated rats. 4 The anorexia is not due to pain or irritative properties of prostaglandin F2a since induction of comparable pain with 3% acetic acid does not affect food intake in rats deprived of food for 22 hours. 5 Anorectic doses of prostaglandin F2a when injected intraperitoneally cause hypothermia.6 The results suggest that the inhibitory activity of prostaglandin F2a on food intake is at both peripheral and central sites. 7 Prostaglandin F2a-induced anorexia is associated with the behavioural tranquillization that is seen after the ingestion of food.

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Hepatic Receptors and the Neurophysiological Mechanisms Controlling Feeding Behavior

Cited by 80 publications

References 136 publications

Anorectic Activity of Prostaglandin Precursors

Anorectic Activity of Prostaglandin Precursors

Substrate oxidation influences liking, wanting, macronutrient selection, and consumption of food in humans

SOME OBSERVATIONS ON THE ANORECTIC ACTIVITY OF PROSTAGLANDIN F_2α

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Hepatic Receptors and the Neurophysiological Mechanisms Controlling Feeding Behavior

Cited by 80 publications

References 136 publications

Anorectic Activity of Prostaglandin Precursors

Anorectic Activity of Prostaglandin Precursors

Substrate oxidation influences liking, wanting, macronutrient selection, and consumption of food in humans

SOME OBSERVATIONS ON THE ANORECTIC ACTIVITY OF PROSTAGLANDIN F2α

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SOME OBSERVATIONS ON THE ANORECTIC ACTIVITY OF PROSTAGLANDIN F_2α