A High-Protein, High-Fat, Carbohydrate-Free Diet Reduces Energy Intake, Hepatic Lipogenesis, and Adiposity in Rats

Pichon, Lisa; Huneau, Jean‐François; Fromentin, Gilles; Tomé, Daniel

doi:10.1093/jn/136.5.1256

Cited by 103 publications

(97 citation statements)

References 16 publications

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“…This nonoxidative glyconeogenic disposal pathway of gluconeogenic substrates copes with amino acid excess and participates in adjusting both amino acid and glucose homeostasis. This pathway may be involved in improving glucose disposal and reducing fat deposition, as previously observed in rats fed a high-protein diet (6,34,46). Further investigations are however, required to verify this hypothesis and to understand the regulatory role of amino acids in this process.…”

Section: Discussionmentioning

confidence: 73%

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Azzout‐Marniche¹,

Gaudichon²,

Blouet³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This paper provides molecular evidence for a liver glyconeogenic pathway, that is, a concomitant activation of hepatic gluconeogenesis and glycogenesis, which could participate in the mechanisms that cope with amino acid excess in high-protein (HP) fed rats. This evidence is based on the concomitant upregulation of phosphoenolpyruvate carboxykinase (PEPCK) gene expression, downregulation of glucose 6-phosphatase catalytic subunit (G6PC1) gene expression, an absence of glucose release from isolated hepatocytes and restored hepatic glycogen stores in the fed state in HP fed rats. These effects are mainly due to the ability of high physiological concentrations of portal blood amino acids to counteract glucagon-induced liver G6PC1 but not PEPCK gene expression. These results agree with the idea that the metabolic pathway involved in glycogen synthesis is dependent upon the pattern of nutrient availability. This nonoxidative glyconeogenic disposal pathway of gluconeogenic substrates copes with amino excess and participates in adjusting both amino acid and glucose homeostasis. In addition, the pattern of PEPCK and G6PC1 gene expression provides evidence that neither the kidney nor the small intestine participated in gluconeogenic glucose production under our experimental conditions. Moreover, the main glucose-6-phosphatase (G6Pase) isoform expressed in the small intestine is the ubiquitous isoform of G6Pase (G6PC3) rather than the G6PC1 isoform expressed in gluconeogenic organs.high-protein diet; glyconeogenesis; glucose 6-phosphatase; phosphoenolpyruvate carboxykinase; liver THE CONSEQUENCES OF HIGH-PROTEIN feeding on the regulation and pathways of glucose disposal through glycogen metabolism and gluconeogenesis remain unclear. High-protein feeding induced both insulin and glucagon secretion in the fed state, associated with the repletion of glycogen stores (3, 45, 52), whereas excess dietary amino acids are metabolized within tissues and the derived nitrogen released into the circulation in the form of glutamine, alanine, serine, and glycine (28, 56). These amino acids are subsequently taken up by the liver, and the nitrogen is converted to urea and glutamine (12,28), the bulk of their carbon skeleton being converted to glucose through hepatic gluconeogenesis (8,29,37,51). This concomitant activation of both glycogen synthesis and gluconeogenesis in the fed state raises the question as to whether the glucose-6-P produced from gluconeogenic amino acid precursors could be directly channeled to glycogen through glycogenesis instead of being excreted as glucose from hepatocytes. This pathway of glyconeogenesis has been discussed over several decades, but despite some evidence during refeeding (49), its significance and molecular basis remain poorly understood (4, 30), and it has not previously been hypothesized under high-protein feeding.It is established that insulin stimulates glycogen synthesis and represses the gluconeogenic production of glucose, whereas glucagon represses glycogen synthesis and stimulates glucose ...

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Section: Discussionmentioning

confidence: 73%

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Azzout‐Marniche¹,

Gaudichon²,

Blouet³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…With HP intake, excess nitrogen needs to be disposed by urea synthesis and glucose must be synthesized de novo (Kuhla et al, 2010) which are highly energy consuming processes. Thus, high protein diets provide less net energy than isoenergetic Control diets (Johnston et al, 2002;Lacroix et al, 2004;Pichon et al, 2006), which is reflected in the lower fat pad mass of dams fed an HP diet during lactation. Maternal kidney mass responded to an HP diet with an increase and in particular in the dams fed an HP diet during gestation and lactation.…”

Section: Discussionmentioning

confidence: 99%

High-protein diet during gestation and lactation affects mammary gland mRNA abundance, milk composition and pre-weaning litter growth in mice

Kucia

Langhammer

Görs

et al. 2011

Animal

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We evaluated the effect of a high-protein diet (HP) on pregnancy, lactational and rearing success in mice. At the time of mating, females were randomly assigned to isoenergetic diets with HP (40% w/w) or control protein levels (C; 20%). After parturition, half of the dams were fed the other diet throughout lactation resulting in four dietary groups: CC (C diet during gestation and lactation), CHP (C diet during gestation and HP diet during lactation), HPC (HP diet during gestation and C diet during lactation) and HPHP (HP diet during gestation and lactation). Maternal and offspring body mass was monitored. Measurements of maternal mammary gland (MG), kidney and abdominal fat pad masses, MG histology and MG mRNA abundance, as well as milk composition were taken at selected time points. HP diet decreased abdominal fat and increased kidney mass of lactating dams. Litter mass at birth was lower in HP than in C dams (14.8 v. 16.8 g). Dams fed an HP diet during lactation showed 5% less food intake (10.4 v. 10.9 g/day) and lower body and MG mass. On day 14 of lactation, the proportion of MG parenchyma was lower in dams fed an HP diet during gestation as compared to dams fed a C diet (64.8% v. 75.8%). Abundance of MG a-lactalbumin, b-casein, whey acidic protein, xanthine oxidoreductase mRNA at mid-lactation was decreased in all groups receiving an HP diet either during gestation and/or lactation. Milk lactose content was lower in dams fed an HP diet during lactation compared to dams fed a C diet (1.6% v. 2.0%). On days 14, 18 and 21 of lactation total litter mass was lower in litters of dams fed an HP diet during lactation, and the pups' relative kidney mass was greater than in litters suckled by dams receiving a C diet. These findings indicate that excess protein intake in reproducing mice has adverse effects on offspring early in their postnatal growth as a consequence of impaired lactational function.

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“…This has been related to greater satiety with high-protein diets, lower insulin levels with low-carbohydrate diets and the energy required to convert amino acids in glucose compounds for gluconeogenesis (107) . High-protein diets were also found to increase cholecystokinin and decrease plasma levels of the orexigenic hormone ghrelin (110,111) , reduce gastric emptying (111) and increase central nervous system leptin sensitivity (109,112) .…”

Section: Energy Densitymentioning

confidence: 99%

High-fat diet-induced obesity in animal models

2010

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Epidemiological studies have shown a positive relationship between dietary fat intake and obesity. Since rats and mice show a similar relationship, they are considered an appropriate model for studying dietary obesity. The present paper describes the history of using high-fat diets to induce obesity in animals, aims to clarify the consequences of changing the amount and type of dietary fats on weight gain, body composition and adipose tissue cellularity, and explores the contribution of genetics and sex, as well as the biochemical basis and the roles of hormones such as leptin, insulin and ghrelin in animal models of dietary obesity. The major factors that contribute to dietary obesity -hyperphagia, energy density and post-ingestive effects of the dietary fat -are discussed. Other factors that affect dietary obesity including feeding rhythmicity, social factors and stress are highlighted. Finally, we comment on the reversibility of high-fat diet-induced obesity.

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A High-Protein, High-Fat, Carbohydrate-Free Diet Reduces Energy Intake, Hepatic Lipogenesis, and Adiposity in Rats

Cited by 103 publications

References 16 publications

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

High-protein diet during gestation and lactation affects mammary gland mRNA abundance, milk composition and pre-weaning litter growth in mice

High-fat diet-induced obesity in animal models

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