Digestive System

Mellinkoff, S

doi:10.1146/annurev.ph.19.030157.001135

Cited by 34 publications

(6 citation statements)

References 107 publications

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“…The present results are also not entirely compatible with the hypothesis that plasma amino acid patterns regulate food intake; the aminostat theory of Almquist (1954) and Mellinkoff (1957). Harper et al (1970) suggested that rats given diets limited or unbalanced with respect to amino acids restrict food intake in order to preserve amino acid homoeostasis.…”

Section: Animals Having Submaximal Rates Of Protein Depositioncontrasting

confidence: 94%

“…If this had simply been due to a low plasma level of the limiting amino acids then one would have expected the rats to eat more. This observation fits the aminostat hypothesis (Almquist, 1954;Mellinkoff, 1957) since at the low rate of growth induced by deficiencies in limiting amino acids, other nonlimiting amino acids would tend to accumulate and this may have induced satiety (Leung & Rogers, 1969;Sanahuja & Harper, 1973). Thus intakes containing IOO g proteinlkg decreased as the efficiency of utilization of dietary N decreased ( Table 7).…”

Section: Animals Having Submaximal Rates Of Protein Depositionsupporting

confidence: 68%

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The effect of varying the quality of dietary protein and energy on food intake and growth in the Zucker rat

Radcliffe¹,

Webster²

1979

Br J Nutr

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I . Food intake and rates of protein, lipid and energy deposition were measured for lean and obese (fatty) Zucker rats offered to appetite from 34 d of age to slaughter at 66 d of age, one of sixteen semi-synthetic diets. Measurements were also made of the digestibility of dietary protein and the metabolizability of dietary energy. Total carcasses were analysed for protein and lipid, and body energy was calculated thereby. Changes in body constituents were calculated by the comparative-slaughter technique.2. In Expt I , four rats of each phenotype and sex were offered one of four diets, each of which contained either I 50 or 300 g casein ( I 50 C and 300 C respectively)/kg and either I 50 or 300 g cellulose ( I 50 CELL and 300 CELL respectively)/kg (diets I 50 C/I 50 CELL, I 50 c/300 CELL, 300 c/ I 50 CELL and 300 C/300 CELL. As expected, males ate more and had higher rates of protein deposition than female animals of the same phenotype on all diets. These sex differences were greater for the lean phenotype. The results for animals in this experiment are presented with, and discussed in relation to, those obtained previously for animals of both sexes fed on cellulose-free diets having these two levels of casein. 3. In Expt 2 , four female animals of each phenotype were fed one of twelve semi-synthetic diets, each of which contained casein, gluten or zein at one of the following levels (g crude protein (nitrogen x 625)/kg diet): 93, 132, 267 or 627. On all diets containing zein both fatty and lean rats had similar, low food intakes and failed to grow. Fatty rats fed on diets containing casein or gluten had higher rates of food intake, weight gain, lipid and energy deposition than lean rats, but similar rates of protein deposition. Rats fed on diets having the two lower levels of casein ate more and grew better than animals of the same phenotype fed on the two corresponding diets containing gluten but at higher protein levels differences in food intake and growth attributable to differences in protein quality disappeared and furthermore, the rate of protein deposition became similar and maximal for both phenotypes.4. The results from both experiments are discussed in relation to previous work on appetite control in the Zucker rat. It appears that fatty and lean rats eat during growth to attain the maximal rate of protein deposition of which they are capable. The rate of lipid deposition would appear to be of no importance in the food intake regulation of animals depositing protein maximally.5. Rats given diets that fail to support maximal rates of protein deposition appear to regulate their intake of digestible energy rather than that of digestible protein. They do not overeat protein-deficient diets in order to acquire sufficient protein for maximal growth although the factors that induce satiety in these animals are unknown.In previous work, congenitally-obese (fatty) and lean Zucker rats of both sexes were given free access during growth to a range of diets whose protein content was varied by altering the propo...

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Section: Animals Having Submaximal Rates Of Protein Depositioncontrasting

confidence: 94%

Section: Animals Having Submaximal Rates Of Protein Depositionsupporting

confidence: 68%

The effect of varying the quality of dietary protein and energy on food intake and growth in the Zucker rat

Radcliffe¹,

Webster²

1979

Br J Nutr

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“…This slow, but precise regulation allows the body weight of an individual to fluctuate around a stable mean [3–4]. Various hypotheses have been put forward as to the feedback signal that would allow body weight to be controlled including mechanisms that regulate blood glucose [5], amino acids [6] or body temperature [7]. In 1953, Kennedy proposed the lipostatic theory [8] in which food intake is controlled by the hypothalamus to regulate body fat stores and over time it has become accepted that changes in the body weight of an adult are primarily determined by changes in body fat mass.…”

Section: 1 Introductionmentioning

confidence: 99%

Direct and indirect effects of leptin on adipocyte metabolism

Harris

2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

253

167

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Leptin is hypothesized to function as a negative feedback signal in the regulation of energy balance. It is produced primarily by adipose tissue and circulating concentrations correlate with the size of body fat stores. Administration of exogenous leptin to normal weight, leptin responsive animals inhibits food intake and reduces the size of body fat stores whereas mice that are deficient in either leptin or functional leptin receptors are hyperphagic and obese, consistent with a role for leptin in the control of body weight. This review discusses the effect of leptin on adipocyte metabolism. Because adipocytes express leptin receptors there is the potential for leptin to influence adipocyte metabolism directly. Adipocytes also are insulin responsive and receive sympathetic innervation, therefore leptin can also modify adipocyte metabolism indirectly. Studies published to date suggest that direct activation of adipocyte leptin receptors has little effect on cell metabolism in vivo, but that leptin modifies adipocyte sensitivity to insulin to inhibit lipid accumulation. In vivo administration of leptin leads to a suppression of lipogenesis, an increase in triglyceride hydrolysis and an increase in fatty acid and glucose oxidation. Activation of central leptin receptors also contributes to the development of a catabolic state in adipocytes, but this may vary between different fat depots. Leptin reduces the size of white fat depots by inhibiting cell proliferation both through induction of inhibitory circulating factors and by contributing to sympathetic tone which suppresses adipocyte proliferation.

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“…Subsequently, imbalanced diets were found to depress food intake and to elevate the plasma levels of lysine, methionine, and threonine (99). Changes in intake were more closely related to changes in PAA levels than to concentration per se (79). Harper (55) found that when high-protein diets were fed to rats, the surplus amino acids, which accounted for the amino acid imbalance, were monitored by an appetite-regulating mechanism.…”

Section: Introductionmentioning

confidence: 99%

Chemical Factors and Their Relation to Feed Intake Regulation in Ruminants: A Review

Jones¹

1972

Can. J. Anim. Sci.

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The subject is reviewed with respect to the role of nutrient metabolism upon the regulation of ruminant feed intake. Chemical factors associated with changes in dietary or nutrient composition and their metabolism within the reticulorumen or animal body, or both, are emphasized. The importance of physical, physiological or metabolic, and sensory regulatory mechanisms are discussed in relation to their effects upon the formation of various metabolites known to be related to feeding. These include volatile fatty acids, amino acids, and blood glucose. Various tissues are discussed in relation to their relative importance for activation of a feedback signal associated with satiety. A general hypothesis is postulated for the integration of various factors, known to influence feed intake regulation, into a complex system.

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Digestive System

Cited by 34 publications

References 107 publications

The effect of varying the quality of dietary protein and energy on food intake and growth in the Zucker rat

The effect of varying the quality of dietary protein and energy on food intake and growth in the Zucker rat

Direct and indirect effects of leptin on adipocyte metabolism

Chemical Factors and Their Relation to Feed Intake Regulation in Ruminants: A Review

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