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Background: We have reported large differences in adiposity (fat mass/body weight) gain between rats fed a low-fat, high-starch diet, leading to their classification into carbohydrate "sensitive" and "resistant" rats. In sensitive animals, fat accumulates in visceral adipose tissues, leading to the suggestion that this form of obesity could be responsible for rapid development of metabolic syndrome., Objective: We investigated whether increased amylase secretion by the pancreas and accelerated starch degradation in the intestine could be responsible for this phenotype., Method: Thirty-two male Wistar rats (7-wk-old) were fed a purified low-fat (10%), high-carbohydrate diet for 6 wk, in which most of the carbohydrate (64% by energy) was provided as corn starch. Meal tolerance tests of the Starch diet were performed to measure glucose and insulin responses to meal ingestion. Indirect calorimetry combined with use of 13C-labelled dietary starch was used to assess meal-induced changes in whole body and starch-derived glucose oxidation. Real-time polymerase chain reaction was used to assess mRNA expression in pancreas, liver, white and brown adipose tissues, and intestine. Amylase activity was measured in the duodenum, jejunum, and ileum contents. ANOVA and regression analyses were used for statistical comparisons., Results: "Resistant" and "sensitive" rats were separated according to adiposity gain during the study (1.73% ± 0.20% compared with 4.35% ± 0.36%). Breath recovery of 13CO2 from 13C-labelled dietary starch was higher in "sensitive" rats, indicating a larger increase in whole body glucose oxidation and, conversely, a larger decrease in lipid oxidation. Amylase mRNA expression in pancreas, and amylase activity in jejunum, were also higher in sensitive rats., Conclusion: Differences in digestion of starch can promote visceral fat accumulation in rats when fed a low-fat, high-starch diet. This mechanism may have important implications in human obesity., (© 2019 American Society for Nutrition.)

Background: Protein status is controlled by the brain, which modulates feeding behavior to prevent protein deficiency., Objective: This study tested in rats whether protein status modulates feeding behavior through brain reward pathways., Methods: Experiments were conducted in male Wistar rats (mean ± SD weight; 230 ± 16 g). In experiment 1, rats adapted for 2 wk to a low-protein (LP; 6% of energy) or a normal-protein (NP; 14% of energy) diet were offered a choice between 3 cups containing high-protein (HP; 50% of energy), NP, or LP feed; their intake was measured for 24 h. In 2 other experiments, the rats were adapted for 2 wk to NP and either HP or LP diets and received, after overnight feed deprivation, a calibrated HP, NP, or LP meal daily. After the meal, on the last day, rats were killed and body composition and blood protein, triglycerides, gut neuropeptides, and hormones were determined. In the brain, neuropeptide mRNAs in the hypothalamus and c-Fos protein and opioid and dopaminergic receptor mRNAs in the nucleus accumbens (NAcc) were measured., Results: Rats fed an LP compared with an NP diet had 7% lower body weight, significantly higher protein intake in a choice experiment (mean ± SD: 30.5% ± 0.05% compared with 20.5% ± 0.05% of energy), higher feed-deprived blood ghrelin, lower postmeal blood leptin, and higher neuropeptide Y (Npy) and corticotropin-releasing hormone (Crh) mRNA expression in the hypothalamus. In contrast to NP, rats fed an LP diet showed postmeal c-Fos protein expression in the NAcc, which was significantly different between meals, with LP < NP < HP. In contrast, in rats adapted to an HP diet compared with an NP diet, energy intake was lower; and in the NAcc, meal-induced c-Fos protein expression was 20% lower, and mRNA expression was 17% higher for dopamine receptor 2 (Drd2) receptors and 38% lower for κ opioid receptor (Oprk1) receptors., Conclusion: A protein-restricted diet induced a reward system-driven appetite for protein, whereas a protein-rich diet reduced the meal-induced activation of reward pathways and lowered energy intake in male rats.

Background: Cooking may impair meat protein digestibility. When undigested proteins are fermented by the colon microbiota, they can generate compounds that potentially are harmful to the mucosa., Objectives: This study addressed the effects of typical cooking processes and the amount of bovine meat intake on the quantity of undigested proteins entering the colon, as well as their effects on the intestinal mucosa., Methods: Male Wistar rats (n = 88) aged 8 wk were fed 11 different diets containing protein as 20% of energy. In 10 diets, bovine meat proteins represented 5% [low-meat diet (LMD)] or 15% [high-meat diet (HMD)] of energy, with the rest as total milk proteins. Meat was raw or cooked according to 4 processes (boiled, barbecued, grilled, or roasted). A meat-free diet contained only milk proteins. After 3 wk, rats ingested a (15)N-labeled meat meal and were killed 6 h later after receiving a (13)C-valine injection. Meat protein digestibility was determined from (15)N enrichments in intestinal contents. Cecal short- and branched-chain fatty acids and hydrogen sulfide were measured. Intestinal tissues were used for the assessment of protein synthesis rates, inflammation, and histopathology., Results: Meat protein digestibility was lower in rats fed boiled meat (94.5% ± 0.281%) than in the other 4 groups (97.5% ± 0.0581%, P < 0.001). Cecal and colonic bacterial metabolites, inflammation indicators, and protein synthesis rates were not affected by cooking processes. The meat protein amount had a significant effect on cecal protein synthesis rates (LMD > HMD) and on myeloperoxidase activity in the proximal colon (HMD > LMD), but not on other outcomes. The ingestion of bovine meat, whatever the cooking process and the intake amount, resulted in discrete histologic modifications of the colon (epithelium abrasion, excessive mucus secretion, and inflammation)., Conclusions: Boiling bovine meat at a high temperature (100°C) for a long time (3 h) moderately lowered protein digestibility compared with raw meat and other cooking processes, but did not affect cecal bacterial metabolites related to protein fermentation. The daily ingestion of raw or cooked bovine meat had no marked effect on intestinal tissues, despite some slight histologic modifications on distal colon., (© 2016 American Society for Nutrition.)

Background: Meat protein digestibility can be impaired because of indigestible protein aggregates that form during cooking. When the aggregates are subsequently fermented by the microbiota, they can generate potentially harmful compounds for the colonic mucosa., Objective: This study evaluated the quantity of bovine meat protein escaping digestion in the human small intestine and the metabolic fate of exogenous nitrogen, depending on cooking processes., Methods: Sixteen volunteers (5 women and 11 men; aged 28 ± 8 y) were equipped with a double lumen intestinal tube positioned at the ileal level. They received a test meal exclusively composed of 120 g of intrinsically (15)N-labeled bovine meat, cooked either at 55°C for 5 min (n = 8) or at 90°C for 30 min (n = 8). Ileal effluents and blood and urine samples were collected over an 8-h period after the meal ingestion, and (15)N enrichments were measured to assess the digestibility of meat proteins and the transfer of dietary nitrogen into the metabolic pools., Results: Proteins tended to be less digestible for the meat cooked at 90°C for 30 min than at 55°C for 5 min (90.1% ± 2.1% vs. 94.1% ± 0.7% of ingested N; P = 0.08). However, the particle number and size in ileal digesta did not differ between groups. The appearance of variable amounts of intact fibers was observed by microscopy. The kinetics of (15)N appearance in plasma proteins, amino acids, and urea were similar between groups. The amount of exogenous nitrogen lost through deamination did not differ between groups (21.2% ± 0.8% of ingested N)., Conclusions: Cooking bovine meat at a high temperature for a long time can moderately decrease protein digestibility compared with cooking at a lower temperature for a short time and does not affect postprandial exogenous protein metabolism in young adults. The study was registered at www.clinicaltrials.gov as NCT01685307., (© 2015 American Society for Nutrition.)

This study focused on the fate of the satiating potency of dietary fibers when solubilized in a fat-containing medium. Fourteen percent of either guar gum (GG) or fructo-oligosaccharide (FOS) or a mixture of the 2 (GG-FOS, 5% GG and 9% FOS) were solubilized in water or an oil emulsion (18-21% rapeseed oil in water, v:v) and administered by gavage to mice before their food intake was monitored. When compared with water (control), only GG-FOS solubilized in water or in the oil emulsion reduced daily energy intake by 21.1 and 14.1%, respectively. To further describe this effect, the meal pattern was characterized and showed that GG-FOS increased satiation without affecting satiety by diminishing the size and duration of meals for up to 9 h after administration independently of the solubilization medium. The peripheral blockade of gut peptide receptors showed that these effects were dependent on the peripheral signaling of cholecystokinin but not of glucagon-like peptide 1, suggesting that anorectic signals emerge from the upper intestine rather than from distal segments. Measurements of neuronal activation in the nucleus of solitary tract supported the hypothesis of vagal satiation signaling because a 3-fold increase in c-Fos protein expression was observed in that nucleus after the administration of GG-FOS, independently of the solubilization medium. Taken together, these data suggest that a mixture of GG and FOS can maintain its appetite suppressant effect in fatty media. Adding these dietary fibers to fat-containing foods might therefore be useful in managing food intake.

Proteins are suspected to have a greater satiating effect than the other 2 macronutrients. After protein consumption, peptide hormones released from the gastrointestinal tract (mainly anorexigenic gut peptides such as cholecystokinin, glucagon peptide 1, and peptide YY) communicate information about the energy status to the brain. These hormones and vagal afferents control food intake by acting on brain regions involved in energy homeostasis such as the brainstem and the hypothalamus. In fact, a high-protein diet leads to greater activation than a normal-protein diet in the nucleus tractus solitarius and in the arcuate nucleus. More specifically, neural mechanisms triggered particularly by leucine consumption involve 2 cellular energy sensors: the mammalian target of rapamycin and AMP-activated protein kinase. In addition, reward and motivation aspects of eating behavior, controlled mainly by neurons present in limbic regions, play an important role in the reduced hedonic response of a high-protein diet. This review examines how metabolic signals emanating from the gastrointestinal tract after protein ingestion target the brain to control feeding, energy expenditure, and hormones. Understanding the functional roles of brain areas involved in the satiating effect of proteins and their interactions will demonstrate how homeostasis and reward are integrated with the signals from peripheral organs after protein consumption.

It has been suggested that high-protein (HP) diets may favor weight management by lowering energy intake and reducing body fat. Whether these effects result from changes in energy metabolism remains unclear. We measured the adaptation of energy metabolism components during 2 wk of HP feeding. Fifty male Wistar rats were switched from a control diet to an HP diet (14 and 55% of protein, respectively) for 1, 3, 6, or 14 d. Energy expenditure (EE) and substrate oxidation were measured by indirect calorimetry in feed-deprived rats and after consumption of a test meal. EE components, including the thermic effect of feeding and activity, were not modified during adaptation to an HP diet. Nutrient oxidation in feed-deprived rats was not affected by HP feeding, except for an early increase in protein oxidation. After 1 d, the postprandial inhibition of lipid oxidation (Lox) was blunted, carbohydrate (CHO) oxidation decreased by one-half, and urea clearance decreased by 66%. Thereafter, CHO oxidation gradually rose, resulting in a null CHO balance. Lox and urea clearance recovered after 3 d of adaptation to an HP diet, while protein oxidation reached a plateau. The postprandial oxidation of CHO counterbalanced the amount of ingested CHO as soon as 3 d, leading to a null postprandial CHO balance. We conclude that the inhibition of de novo lipogenesis from dietary CHO, but not EE and Lox, may participate in limiting the adiposity induced by HP feeding. The transient changes occurring during the period of adaptation to the diet highlight that the duration of the diet is critical in HP diet studies.

Dietary protein and amino acids, including glutamate, generate signals involved in the control of gastric and intestinal motility, pancreatic secretion, and food intake. They include postprandial meal-induced visceral and metabolic signals and associated nutrients (eg, amino acids and glucose), gut neuropeptides, and hormonal signals. Protein reduces gastric motility and stimulates pancreatic secretions. Protein and amino acids are also more potent than carbohydrate and fat in inducing short-term satiety in animals and humans. High-protein diets lead to activation of the noradrenergic-adrenergic neuronal pathway in the brainstem nucleus of the solitary tract and in melanocortin neurons of the hypothalamic arcuate nucleus. Moreover, some evidence indicates that circulating concentrations of certain amino acids could influence food intake. Leucine modulates the activity of energy and nutrient sensor pathways controlled by AMP-activated protein kinase and mammalian target of rapamycin in the hypothalamus. At the brain level, 2 afferent pathways are involved in protein and amino acid monitoring: the indirect neural (mainly vagus-mediated) and the direct humoral pathways. The neural pathways transfer preabsorptive and visceral information through the vagus nerve that innervates part of the orosensory zone (stomach, duodenum, and liver). Localized in the brainstem, the nucleus of the solitary tract is the main projection site of the vagus nerve and integrates sensory information of oropharyngeal, intestinal, and visceral origins. Ingestion of protein also activates satiety pathways in the arcuate nucleus, which is characterized by an up-regulation of the melanocortin pathway (alpha-melanocyte-stimulating, hormone-containing neurons) and a down-regulation of the neuropeptide Y pathway.

Our objective was to study the relationship between the satiety induced by high-protein meals and the activation of brain areas involved in the onset of satiety. In rats, we used immunohistochemistry to monitor brain centers activated by a meal by receiving information from the gastrointestinal tract or via humoral pathways. In the nucleus of the solitary tract (NTS), the acute or chronic intake of high-protein meals led to increased activation of the noradrenergic/adrenergic neurons involved in cholecystokinin-induced satiety. In the arcuate nucleus of the hypothalamus, the melanocortin pathway was also more strongly activated after the acute or chronic intake of high-protein meals. Moreover, the glucagon-like peptide 1 pathway arising from the NTS, which is triggered, among other behaviors, during nonphysiological anorexia, was not activated by high-protein meals, supporting the lack of aversive behavior associated with this diet. Taken together, these results show that the ability of high-protein meals to inhibit food intake occurs alongside the activation, in nutrient-sensitive brain areas, of several specific neuronal populations involved in satiety.

This study was designed to characterize the suppressant effect of yeast protein and purified peptides on energy intake. For this purpose, 5 experiments were carried out using adult male Wistar rats. Rats that consumed ad libitum a standard yeast protein diet ate significantly less and were leaner over 21 d than rats that consumed ad libitum a standard milk protein diet (Expt. 1). Moreover, rats fed a high yeast protein load reduced their next meal and daily energy intake more than rats fed any other well-balanced, amino acid, high protein load (soy, total milk protein, or wheat gluten) and more than those fed a wheat starch diet (Expt. 2). Purified peptides from the yeast protein extract produced similar effects on subsequent energy intake (Expt. 3). Study of the behavioral satiety sequence showed that rats consuming P14-y or P55-y diets ad libitum did not acquire a conditioned food aversion (Expt. 4). Finally, a preliminary study of gastric emptying in rats fed yeast protein loads showed that yeast protein was emptied more rapidly through the pylorus than total milk protein during a meal, which may induce satiety (Expt. 5). Taken together, these experiments show that yeast proteins enhance satiety in rats more than other proteins.

The aim of this work was to determine the effects in rats of ingesting 1 of 3 diets with normal or high protein concentrations and various carbohydrate:lipid ratios on weight gain, body composition, and the development and metabolism of white adipose tissue (WAT). For this purpose, male Wistar rats were fed for 20 or 42 d a high-carbohydrate, low-fat, normal-protein diet (76, 10, and 14% of energy as carbohydrate, lipid, and protein, respectively, carbohydrate:lipid ratio (C/L) = 7.6), a normal-carbohydrate, low-fat, high-protein diet (35, 10, and 55% of energy as carbohydrate, lipid, and protein respectively, C:L = 3.5), or a carbohydrate-free, high-fat, high-protein diet (45 and 55% of energy as fat and protein, respectively, C:L = 0). Growth, food intake, body composition, WAT cellularity, and several markers of lipogenesis including fatty acid synthase and lipoprotein lipase activities were measured in adipose tissue and liver. Lowering the C:L ratio reduced the development of WAT, weight gain, body fat mass, and adipocyte size, and in rats fed the carbohydrate-free diet (C:L = 0), the total number of adipocytes in subcutaneous WAT. These reductions in adipose tissue development with decreases in the C:L ratio of the diet seemed to be due primarily to reduced hepatic lipogenesis.

Transition from a normal- (NP) to a high-protein (HP) diet induces a rapid depression in food intake and a progressive but incomplete return to the initial intake during the succeeding days. The aim of this study was to determine which CNS regions are involved in the HP diet-induced satiety in rats. Brains were collected from 3 groups of adult rats after habituation to an NP diet (21 d), during the transition phase to a HP diet (2 d), or after habituation to the HP diet (21 d). Fos expression was measured in several brain areas that are involved in the control of food intake (solitary tract nucleus, anterior piriform cortex, lateral hypothalamus, arcuate nucleus, posterior para ventricular nucleus, medio ventral hypothalamus, dorso medial hypothalamus, amygdala, and accumbens nucleus). Changes occurred in the majority of these regions during the transition period from the NP diet to the HP diet. After habituation to the HP diet, significant changes in Fos expression were restricted to an increase in the nucleus of the solitary tract and a decrease in the ventromedial hypothalamus and the cortex of the amygdala. Considering the functional characteristics of these areas, the present results suggest that the vagus nerve conveys the information relative to the quantity of protein ingested, that hypothalamic sites regulate food intake and may alter sympathetic nervous system activity, and that higher brain functions such as memory processing by the limbic system or food reward system are involved in the HP diet-induced satiety in rats.

The purpose of the present study was to test the influence of the amount of protein in a carbohydrate-free diet during a weight reducing program using severe (75%) or more moderate (35%) energy restriction in rats. In Expt. 1, 3 groups (n = 6) consumed ad libitum a high-carbohydrate, low-fat diet [P21C69L10 containing 21% of energy as protein (P21), 69% carbohydrate (C69) and 10% lipids (L10)], a high-carbohydrate, high-fat diet (P21C34L45), or a carbohydrate-free, high-fat, high-protein diet (P55L45). In Expt. 2, 7 groups (n = 7) were studied. For 20 d, groups 1-4 consumed ad libitum diets containing macronutrients at the proportions indicated in their designations [P14C56L30 (control diet), P30L70, P50L50, and P90L10]. Groups 5-7 were pair-fed the same diets at the level of the spontaneous intake of the P90L10 group on the previous day (35% energy restriction). In Expt. 3, 5 groups (n = 7) were fed 1 of the following diets for 20 d. Group 1 consumed the control diet (P14C56L30) ad libitum. Groups 2-5 were energy restricted to 25% of the daily energy intake of group 1 with diets varying in their protein and lipid concentrations (P14C56L30, P50L50, P70L30, and P90L10). A high-fat content in the diet devoid of carbohydrate did not increase energy intake and body adiposity and neither body weight nor body composition was significantly affected by the protein to lipid ratio when energy restriction was 75%; however, a protein content > 50% preserved lean body mass at the expense of fat mass when energy restriction was 35%. Our results show that the absence of carbohydrates from the diet induces a low energy intake and the preferential deposition of protein.

This study was designed to assess the effects of transition and adaptation to a very high protein diet on behavioral food responses, energy intake, body weight gain, and body composition in rats. For this purpose, adult male Wistar rats were fed either a diet with 70% of energy as protein (P70 group) or a diet with 14% of energy as protein (P14 group) for 16 d. These two groups were compared with a P14 pair-fed (P14-pf) group. A behavioral satiety sequence was also examined. The P70 group ate 21% less than the P14 rats (P < 0.001) and gained less body weight (P < 0.01). The P70 group gained more carcass weight than either P14 or P14-pf rats (P < 0.05). Behavior and food intake data were affected in P70 rats on d 1 of eating the very high protein diet and then returned to baseline values as early as d 2 of consuming the P70 diet. Rats that adapted to the very high protein diet did not acquire a conditioned taste aversion but rather exhibited satiety and a normal behavioral satiety sequence.

Rats that are allowed to select their diets [dietary self- selection (DSS)] often ingest >30% of their daily energy in the form of protein. Such an intake may seem unhealthy, but the consistency of this choice suggests that it is motivated by physiologic drives. To gain a clearer understanding of how protein selection is structured during DSS, we adapted 12 rats to a standard diet (14% Protein) and then allowed them to choose between two diets, i.e., total milk protein (P) and a mix of carbohydrates and lipids (FC). The protein intake during DSS rose above 40%; assuming an intermeal interval of 10 min, 70% of the energy intake occurred with meals that included both P and FC, with the sequence of FC followed by P preferred to the sequence of P followed by FC (70 vs. 30%, P < 0.001). In addition, energy intake during the light period was reduced to only 10% of the daily energy intake [vs. 30% with the control P14 diet or a with a high-protein diet (50%)], and 90% of the intake was in the form of pure protein meals. In complementary studies, we verified that the high protein intake also occurred when rats were offered casein and whey and was not due to the high palatability of the milk protein. We conclude that a specific feeding pattern accompanies high protein intake in rats allowed DSS. The mechanisms underlying this behavior and its potential beneficial/adverse consequences over the long term still must be clarified.

This study was undertaken to determine whether the subdiaphragmatic vagus nerve is involved in the depression of food intake induced by the ingestion of a high protein diet (P50) in rats. After total subdiaphragmatic vagotomy (Vago group) or sham surgery (Sham group), rats consumed the control diet for a 2-wk recovery period and then both groups consumed the high protein diet for 16 d. Daily food intake, meal pattern analysis and behavioral satiety sequence were measured. Total subdiaphragmatic vagotomy did not modify the daily intake of the control diet or suppress the dramatic depression in food intake produced by acute transition to a high protein diet. However, the daily intake of a high protein diet was slightly reduced under acute conditions or even after adaptation (P < 0.005). Analysis of meal parameters and the behavioral satiety sequence after adaptation indicated no major metabolic distress. In conclusion, these results suggest that the subdiaphragmatic vagus nerve does not constitute an obligatory pathway for the transfer of information to the brain, resulting in a depression of high protein diet intake. In contrast, a defect in this visceral regulating system could reinforce the metabolic-associated food intake depression signal.

Background: Dietary fat composition is thought to affect body weight regulation independent of the amount of fat ingested., Objective: We analyzed the feeding behavior, body weight gain, body composition, and energy metabolism in lean and obese rats fed a diet in which fat was in the form of either butter or soybean oil., Design: Ten lean (Fa/?) and 10 obese (fa/fa) adult Zucker rats were divided into 4 groups according to a 2 x 2 experimental design. They were fed a normally balanced diet over 11 wk in which 30% of energy was either soybean oil or butter. Food intake, body weight gain, and body composition were measured. Indirect calorimetry was used to study energy metabolism at rest and in relation to feeding and activity., Results: Food intake increased similarly in lean and obese rats after butter feeding. Body weight gain increased in obese rats and decreased in lean rats after butter feeding. Body weight gain in obese rats was due mainly to an increase in the weight of lean tissues besides muscle, whereas adiposity and distribution of fat between the various pads did not change. Resting metabolic rates and postprandial lipid oxidation increased in butter-fed obese rats. Lipid oxidation during exercise was not significantly different between obese and lean rats. Fat oxidation increased in butter-fed lean rats during treadmill running at moderate intensity., Conclusions: In obese rats, basal metabolism and postprandial lipid oxidation increased during butter feeding, which appeared to prevent fat accumulation in the long term. In lean rats, butter feeding favored lipid utilization by working muscles, an observation that deserves further investigation in terms of endurance and performance.