Effects of Quantity and Quality of Dietary Protein and Variation in Certain Enzyme Activities on Glucose Metabolism in the Rat

Péret, J; Chanez, Marc; J, Cota; Macaire, I

doi:10.1093/jn/105.12.1525

Cited by 31 publications

(18 citation statements)

References 38 publications

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“…This effect is observed with diet containing protein or not carbohydrates suggesting that the level of protein per se in the diet is able to stimulate hepatic gluconeogenesis. 42,43 Interestingly, when increasing the protein content of the diet, PEPCK (which controls the initial conversion of oxaloacetate to phosphoenolpyruvate) is upregulated either in the fasted and in the fed state, whereas glucose 6-phosphatase (G6Pase) (which controls the last step of gluconeogenesis) is upregulated in the fasted state and downregulated in the fed state. 43,44 These observations strongly suggest that liver gluconeogenesis is stimulated by a high-protein diet but that in the fed state the newly synthesized glucose 6-phosphate (G6P) is directed toward glycogen synthesis whereas in the fasted state it is converted to glucose and released from hepatocyte.…”

Section: Gluconeogenesismentioning

confidence: 99%

“…42,43 Interestingly, when increasing the protein content of the diet, PEPCK (which controls the initial conversion of oxaloacetate to phosphoenolpyruvate) is upregulated either in the fasted and in the fed state, whereas glucose 6-phosphatase (G6Pase) (which controls the last step of gluconeogenesis) is upregulated in the fasted state and downregulated in the fed state. 43,44 These observations strongly suggest that liver gluconeogenesis is stimulated by a high-protein diet but that in the fed state the newly synthesized glucose 6-phosphate (G6P) is directed toward glycogen synthesis whereas in the fasted state it is converted to glucose and released from hepatocyte. The control of PEPCK and G6Pase activity in the liver by nutrients has a profound impact on hepatic metabolism and glucose homeostasis 45,46 and the satiating effect of high-protein feeding could be related to the improvement of glucose homeostasis through the modulation of hepatic gluconeogenesis and subsequent glucose metabolism.…”

Section: Gluconeogenesismentioning

confidence: 99%

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Dietary protein, metabolism, and body-weight regulation: dose–response effects

et al. 2006

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Body-weight management requires a multifactorial approach. Recent findings suggest that an elevated protein intake seems to play a key role herein, through (i) increased satiety related to increased diet-induced thermogenesis; (ii) its effect on thermogenesis; (iii) body composition; and (iv) decreased energy-efficiency, all of which are related to protein metabolism. Supported by these mechanisms, relatively larger weight loss and subsequent stronger body-weight maintenance have been observed. Increased insulin sensitivity may appear, but it is unclear whether this is due to weight loss or type of diet. The phenomenon of increased satiety is utilized in reduced energy-intake diets, mainly in the ad libitum condition, whereby sustained satiety is achieved with sustained absolute protein intake in grams, despite lower energy intake. Elevated thermogenesis and glucagon-like peptide-1 (GLP-1) appear to play a role in high-protein induced satiety. Under conditions of weight maintenance, a high-protein diet shows a reduced energy efficiency related to the body composition of the body weight regained, that is, in favor of fat-free mass. Indeed, during body-weight loss, as well as during weight regain, a high-protein diet preserves or increases fat-free mass and reduces fat mass and improves the metabolic profile. In the short-term this may be supported by a positive protein and a negative fat balance, through increased fat oxidation. As protein intake is studied under various states of energy balance, absolute and relative protein intake needs to be discriminated. In absolute grams, a normal protein diet becomes a relatively high-protein diet in negative energy balance and at weight maintenance. Therefore, 'high protein negative energy balance diets' aim to keep the grams of proteins ingested at the same level as consumed at energy balance, despite lower energy intakes.

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Section: Gluconeogenesismentioning

confidence: 99%

Section: Gluconeogenesismentioning

confidence: 99%

Dietary protein, metabolism, and body-weight regulation: dose–response effects

et al. 2006

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“…The nutritional status preceding the fasting period can also modify the metabolic response of the entire organism or of liver gluconeogenesis or ketogenesis (Belo, Romsos and Leveille, 1976 ;Bouchat, Doiz6 and Paquay, 1980 ;Brady et al, 1977 ;Cowan, Vranic and Wrenshall, 1969 ;Mc Donald and Johnson, 1965 ;P6gorier et al, 1982 ;Peret et al, 1975). Few Glycemia and insulinemia were shown to increase in the fed state in rats given a high-fat diet (Portha, Giroix and Picon, 1982).…”

Section: Introductionmentioning

confidence: 99%

Effects of dietary lipid level on ketonemia and other plasma parameters related to glucose and fatty acid metabolism in the rabbit during fasting

Jean-Blain¹,

Durix²

1985

Reprod. Nutr. Dévelop.

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Summary. The effects of a high-fat diet on ketonemia and other plasma parameters of gluconeogenesis and ketogenesis were studied in rabbits during feeding, during a 4-day fast, and again during refeeding. Arterial plasma glucose, lactate, total aminoacids, ketone bodies, insulin and glucagon were measured daily. In the fed state, the high-fat diet induced an increase in plasma NEFA and ketone bodies and a decrease in alaninemia. The most striking effect of the high-fat diet, compared with the normal low-fat diet, was the twofold increase of ketonemia during fasting, even though the difference in NEFA level after both diets was only 19 %. This effect was maintained throughout the fasting period. The high-fat diet also induced higher glycemia and lower alaninemia during further fasting. Insulinemia sharply decreased to a very low value from the beginning of fasting, but the high-fat diet did not have any particular effect. Glucagonemia was not different in the fed state than in fasting, whatever preceding diet was given. Therefore, the lipid content of the diet prior to fasting introduced important and persistent modifications in the triglycerides and glucose metabolism during fasting.Introduction.

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“…De nombreux travaux montrent les effets des régimes riches en protéines sur l'activité des enzymes impliquées dans différentes voies métaboliques (Harper, 1965 ; Szepesi, 1971 (Munro, 1964;Peret et al, 1975 Bucolo, 1974). En outre, elles dépendent de la concentration en glucose ou en glucose-6-phosphate (G6P) des cellules hépatiques, l'ensemble du système étant contrôlé par différentes hormones (insuline, glucagon, catécholamines, etc.)…”

Section: Introductionunclassified

“…2 phosphoglycérate -G6P -glucose) et l'activité de la PK est progressivement inhibée (Weber, 1969 ;Hers, 1976). Lorsque la consommation de nourriture approche le niveau initial, ces phénomènes se stabilisent; l'activité de la PK devient constante et est d'autant plus basse que le régime est plus riche en protéines (Krebs et Eggleston, 1965 ;Peret et al, 1975). …”

Section: Introductionunclassified