Search

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Obesityprone (OP) rodents are used as models of human obesity predisposition. The goal of the present study was to identify preexisting defects in energy expenditure components in OP rats. Two studies were performed. In the first one, male Wistar rats (n 48) were fed a high-carbohydrate diet (HCD) for 3 wk and then a high-fat diet (HFD) for the next 3 wk. This study showed that adiposity gain under HCD was 2.9-fold larger in carbohydrate-sensitive (CS) than in carbohydrate- resistant (CR) rats, confirming the concept of "carbohydratesensitive" rats. Energy expenditure (EE), respiratory quotient (RQ), caloric intake (CI), and locomotor activity measured during HFD identified no differences in EE and RQ between fat-resistant (FR) and fat-sensitive (FS) rats, and indicated that obesity developed in FS rats only as the result of a larger CI not fully compensated by a parallel increase in EE. A specific pattern of spontaneous activity, characterized by reduced activity burst intensity, was identified in FS rats but not in CS ones. This mirrors a previous observation that under HCD, CS but not FS rats, exhibited bursts of activity of reduced intensity. In a second study, rats were fed a HFD for 3 wk, and the components of energy expenditure were examined by indirect calorimetry in 10 FR and 10 FS rats. This study confirmed that a low basal EE, reduced thermic effect of feeding, defective postprandial energy partitioning, or a defective substrate utilization by the working muscle are not involved in the FS phenotype. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the contribution of dietary amino acids (AA) to energy metabolism under high protein (HP) diets, using a double tracer method to follow simultaneously the metabolic fate of α-amino groups and carbon skeletons. Sixty-seven male Wistar rats were fed a normal (NP) or HP diet for 14 days. Fifteen of them were equipped with a permanent catheter. On day 15, after fasting overnight, they received a 4-g meal extrinsically labeled with a mixture of 20 U-[N]-[C] AA. Energy metabolism, dietary AA deamination and oxidation and their transfer to plasma glucose were measured kinetically for 4 h in the catheterized rats. The transfer of dietary AA to liver glycogen was determined at 4 h. The digestive kinetics of dietary AA, their transfer into liver AA and proteins and the liver glycogen content were measured in the 52 other rats that were killed sequentially hourly over a 4-h period. [N] and [C] kinetics in the splanchnic protein pools were perfectly similar. Deamination increased fivefold in HP rats compared to NP rats. In the latter, all deaminated AA were oxidized. In HP rats, the oxidation rate was slower than deamination, so that half of the deaminated AA was non-oxidized within 4 h. Non-oxidized carbon skeletons were poorly sequestrated in glycogen, although there was a significant postprandial production of hepatic glycogen. Our results strongly suggest that excess dietary AA-derived carbon skeletons above the ATP production capacity, are temporarily retained in intermediate metabolic pools until the oxidative capacities of the liver are no longer overwhelmed by an excess of substrates. [ABSTRACT FROM AUTHOR]

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 114 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. [ABSTRACT FROM AUTHOR]

The antipsychotic drug, olanzapine, often induces weight gain and glucose metabolism disturbances, which may result from feeding pattern abnormalities. The objectives of the study were to examine the effects of a chronic olanzapine treatment on feeding patterns in the rat and to investigate a potential time-related association between feeding patterns and the appearance of glucose metabolism abnormalities and adiposity. Male rats were treated with olanzapine (2 mg/kg/day), haloperidol (1 mg/kg/day) or a control solution (drugs mixed with the food). In experiment 1, treatments lasted 26 days and feeding patterns were measured on day 21. In experiment 2, treatments lasted for 46 days, and an oral glucose tolerance test (OGTT) was realised on day 31. At the end of both experiments, plasma parameters and body composition were analysed. In experiment 1, olanzapine-treated animals showed increased meal number, decreased ingestion rate, meal size and inter-meal interval, and no change in total food intake. Plasma glucose, OGTT and body composition were not altered. In experiment 2, after 31 days of treatment, fasting blood glucose was increased and OGTT indicated an insulin resistance. After 46 days of treatment, hyperglycaemia was aggravated (compared to 31 days), and adiposity was increased in olanzapine-treated animals. In both experiments, the haloperidol-treated rats did not differ from the control ones. Chronic olanzapine treatment produces changes in feeding patterns, in a way consistent with an increased incentive drive to eat. As a whole, the results raise the hypothesis that long-term alteration of feeding pattern by olanzapine may predispose to disturbances in the regulation of energy metabolism. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The ingestion of low or high lipid diets enriched with fructo-oligosaccharide (FOS) affects energy homeostasis. Ingesting protein diets also induces a depression of energy intake and decreases body weight. The goal of this study was to investigate the ability of FOS, combined or not with a high level of protein (P), to affect energy intake and body composition when included in diets containing different levels of lipids (L). We performed two studies of similar design over a period of 5 weeks. During the first experiment (exp1), after a 3-week period of adaptation to a normal protein-low fat diet, the rats received one of the following four diets for 5 weeks (6 rats per group): (i) normal protein (14% P/E (Energy) low fat (10% L/E) diet, (ii) normal protein, low fat diet supplemented with 10% FOS, (iii) high protein (55%P/E) low fat diet, and (iv) high protein, low fat diet supplemented with 10% FOS. In a second experiment (exp2) after the 3-week period of adaptation to a normal protein-high fat diet, the rats received one of the following 4 diets for 5 weeks (6 rats per group): (i) normal protein, high fat diet (35% of fat), (ii) normal protein, high fat diet supplemented with 10% FOS, (iii) high protein high fat diet and (iv) high protein high fat diet supplemented with 10% FOS. In low-fat fed rats, FOS did not affect lean body mass (LBM) and fat mass but the protein level reduced fat mass and tended to reduce adiposity. In high-fat fed rats, FOS did not affect LBM but reduced fat mass and adiposity. No additive or antagonistic effects between FOS and the protein level were observed. FOS reduced energy intake in low-fat fed rats, did not affect energy intake in normal-protein high-fat fed rats but surprisingly, and significantly, increased energy intake in high-protein high-fat fed rats. The results thus showed that FOS added to a high-fat diet reduced body fat and body adiposity. [ABSTRACT FROM AUTHOR]

Yeast-derived peptides were previously shown to display a high satiating effect. This work evaluate their effect i) on food intake in rats as well as in humans, and ii) on the activation of brain neuronal pathways involved in food intake including the Nucleus of the Tractus Solitary (NTS) and the Arcuate Nucleus of the Hypothalamus (Arc). Food intake in rats and humans: The ingestion of a daily load of yeast peptides induced a decrease in daily food intake in rats and in humans after a two-week habituation period. This decrease did not occurred during the meal following the load (lunch in humans) but several hours later in rats (-16% of control group daily intake) and during the diner in humans (-13% of control group daily intake). Activation of neuronal pathways in rats: After habituation period, yeast protein loads induced an increase in melanocortin pathway within the Arc, which regulates long-term energy intake, whereas activation of the Glucagon Like Peptide-1 (GLP-1) pathway within the NTS, which is triggered during aversive-induced anorexia, was not increased. Conclusion: Yeast peptides induced a strong food intake suppressing effect in rats and in humans. This effect was not compensated during the rest of the day and did not disappear after habituation. It did not result from a conditioned taste aversion and might be related to a stronger activation of arcuate melanocortin pathway. [ABSTRACT FROM AUTHOR]

The relationship between the satiety induced by high protein meals and activation of brain areas involved in satiety onset remains incompletely understood. We monitored neuronal pathways in brain centres known to be activated by a meal including the Nucleus of the Tractus Solitary (NTS) and the Arcuate Nucleus of the Hypothalamus (Arc) receiving information from gastrointestinal tract and from the blood, respectively. In the NTS, compared to a normal protein diet, acute or chronic intake of a high protein diet increased activation of the noradrenergic/adrenergic pathway known to be involved in cholecystokinin (CCK) induced satiety, but not the Glucagon Like Peptide I (GLP-1) pathway, which is triggered during aversive-induced anorexia. In the ARC, the melanocortin pathway also presented a greater activation after acute or chronic intake of high protein meals. Taken together, these results indicated that the potency of high protein meals in inhibiting food intake was occurring along with the activation of several specific brain neural pathways involved in satiety and not in aversive behaviour. [ABSTRACT FROM AUTHOR]

Focuses on the stability of dietary nitrogen delivery in the periphery of rats adapted to protein intake. Suppression of amino acids reaching the periphery; Role of digestive kinetics and splanchnic anabolism in dietary regulation processes.

Abstract: Brain-derived neurotrophic factor (BDNF) and its TrkB receptor play critical roles in the synaptic activity and plasticity of mature neurons and enhance adult neurogenesis. Furthermore, treatment with BDNF has been found to attenuate weight gain or even cause weight loss and appetite suppression in rats. The aim of this study was to look at the effect of nutrient intake on BDNF concentrations and cellular proliferation in the brain. Adult male Wistar rats were given one of three diets for 6 weeks: high-carbohydrate, high-fat or high-fat pair-fed diets. Rats were sacrificed at the end of the feeding period and BDNF concentrations in the dorsal vagal complex (DVC), hypothalamus and plasma were measured by ELISA on protein extracts of these samples. Cellular proliferation in the DVC was quantified by Ki-67 immunohistochemistry. Neither BDNF levels nor proliferation were modified by the diet. Secondly, using rats that received the same diets, real-time PCR was performed in the DVC, hypothalamus and nodose ganglia in order to compare TrkB receptor levels. The results showed significantly lower TrkB levels in the hypothalamus and nodose ganglia of fasted rats receiving the high-fat diet when compared to the other groups. These two complementary methodological approaches suggest that there is a relationship between long-term dietary intake and BDNF. More precisely, TrkB expression is more responsive to energy states than to diet composition. An increment in energy stores thus triggers decreased BDNF anorexigenic signaling at the receptor level in the hypothalamus and nodose ganglia, but not in the DVC. [Copyright &y& Elsevier]