Julien Piedcoq

Milk protein fractions moderately extend the duration of satiety compared with carbohydrates independently of their digestive kinetics in overweight subjects.

Digestive kinetics are believed to modulate satiety through the modulation of nutrient delivery. We hypothesised that the duration of satiety could be extended by modulating the kinetics of dietary amino acid delivery in overweight subjects, using snacks containing casein and whey protein. In the present study, eighty-two subjects underwent a first satiety test where they received a control snack containing 60 g maltodextrin. For the next 5 d, the subjects consumed a liquid protein snack containing 30 g carbohydrates and 30 g proteins (casein, whey protein or an equal mix of the two; n 26-28 per group). The subjects then underwent a second satiety test after ingesting the protein snack. The time period elapsing between the snack and request for lunch, food intake at lunch and satiety scores were recorded. A subgroup of twenty-four subjects underwent a digestive and metabolic investigation after ingesting their protein snack. Gastric emptying times were 2·5, 4 and 6 h for whey protein, mix and casein, respectively, displaying different kinetics of appearance of dietary N in plasma but without affecting pancreatic and gastrointestinal hormones. Compared with the control snack, proteins extended the duration of satiety (+17 min, P= 0·02), with no difference between the protein groups. The satiating effect of proteins was greater in subjects who ate their lunch early after the snack (below the median value, i.e. 2 h) at the control test (+32 min, P= 0·001). Energy intake at lunch was not modulated by proteins. The satiating effect of proteins is efficient in overweight subjects, especially when the duration of satiety is short, but independently of their digestive and plasma amino acid kinetics.

High dietary protein decreases fat deposition induced by high-fat and high-sucrose diet in rats

High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver.

The satiating effects of eggs or cottage cheese are similar in healthy subjects despite differences in postprandial kinetics

Studies have reported a better satiating effect of eggs when compared with common cereal-based breakfasts, an effect that can be attributed to their macronutrient composition. Our aim was to compare the satiating power of an omelette and cottage cheese, both being common food snacks with similar nutrient compositions (containing proteins and lipids) but in different food forms. Thirty healthy volunteers participated in a randomized crossover trial. On each test day, the subjects consumed one of the two snacks, both providing 1346 kJ, 26 g protein, 21 g lipids, and 8 g lactose. The elapsed time between the snack and lunch request, their food intake at lunch, and their satiety scores were recorded. In a subgroup of 10 volunteers, blood was sampled to measure plasma metabolites and hormones. The two preloads were similar in terms of the time between the snack and a request for the buffet (167 ± 8 min), energy intake at the buffet (3988 ± 180 kJ) and appetite ratings. Plasma amino acid and urea concentrations indicated a marked delay in kinetic delivery after the eggs compared with the cottage cheese. In contrast, glucose, triglycerides and cholesterol displayed similar profiles after the snack. GIP and insulin secretions increased significantly after the cottage cheese, while glucagon and GLP-1 secretions were delayed with the omelette. We conclude that despite important differences in protein kinetics and their subsequent effects on hormone secretion, eggs and cottage cheese had a similar satiating power. This strongly suggests that with dose of proteins that is compatible to supplement strategies, i.e. 20-30 g, a modulation of protein kinetics is ineffective in increasing satiety.

Energy restriction only slightly influences protein metabolism in obese rats, whatever the level of protein and its source in the diet

BACKGROUND High protein (HP) diets during energy restriction have been studied extensively regarding their ability to reduce body fat and preserve lean body mass, but little is known about their effects on protein metabolism in lean tissues. OBJECTIVE To determine the effects of energy restriction and protein intake on protein anabolism and catabolism in rats. METHODS For 5 weeks, 56 male Wistar rats were fed an obesity induction (OI) diet . They were then subjected to a 40% energy restriction using the OI diet or a balanced HP diet for 3 weeks, whereas a control group was fed the OI diet ad libitum (n=8 per group). HP-restricted rats were divided into five groups differing only in terms of their protein source: total milk proteins, casein (C), whey (W), a mix of 50% C and W, and soy (n=8). The animals were then killed in the postprandial state and their body composition was determined. Protein synthesis rates were determined in the liver, gastrocnemius and kidney using a subcutaneous (13)C valine flooding dose. mRNA levels were measured for key enzymes involved in the three proteolysis pathways. RESULTS Energy restriction, but not diet composition, impacted weight loss and adiposity, whereas lean tissue mass (except in the kidney) was not influenced by diet composition. Levels of neoglucogenic amino acids tended to fall under energy restriction (P<0.06) but this was reversed by a high level of protein. The postprandial protein synthesis rates in different organs were similar in all groups. By contrast, mRNA levels encoding proteolytic enzymes rose under energy restriction in the muscle and kidney, but this was counteracted by a HP level. CONCLUSIONS In adult obese rats, energy restriction but not diet composition affected fat pads and had little impact on protein metabolism, despite marked effects on proteolysis in the kidney and muscle.

[13C] GC–C-IRMS analysis of methylboronic acid derivatives of glucose from liver glycogen after the ingestion of [13C] labeled tracers in rats

We developed a complete method to measure low [(13)C] enrichments in glycogen. Fourteen rats were fed a control diet. Six of them also ingested either [U-(13)C] glucose (n=2) or a mixture of 20 [U-(13)C] amino acids (n=4). Hepatic glycogen was extracted, digested to glucose and purified on anion-cation exchange resins. After the optimization of methylboronic acid derivatization using GC-MS, [(13)C] enrichment of extracted glucose was measured by GC-C-IRMS. The accuracy was addressed by measuring the enrichment excess of a calibration curve, which observed values were in good agreement with the expected values (R=0.9979). Corrected delta values were -15.6+/-1.6 delta(13)C (per thousand) for control rats (n=8) and increased to -5 to 8 delta(13)C (per thousand) per thousand and 12-14 delta(13)C (per thousand) per thousand after the ingestion of [U-(13)C] amino acids or [U-(13)C] glucose as oral tracers, respectively. The method enabled the determination of dietary substrate transfer into glycogen. The sequestration of dietary glucose in liver glycogen 4 h after the meal was 35% of the ingested dose whereas the transfer of carbon skeletons from amino acids was only 0.25 to 1%.

Rats Prone to Obesity Under a High-Carbohydrate Diet have Increased Post-Meal CCK mRNA Expression and Characteristics of Rats Fed a High-Glycemic Index Diet

We previously reported that rats prone to obesity exhibit an exaggerated increase in glucose oxidation and an exaggerated decline in lipid oxidation under a low-fat high-carbohydrate (LF/HC) diet. The aim of the present study was to investigate the mechanisms involved in these metabolic dysregulations. After a 1-week adaptation to laboratory conditions, 48 male Wistar rats were fed a LF/HC diet for 3 weeks. During weeks 2 and 3, glucose tolerance tests (GTT), insulin tolerance tests (ITT), and meal tolerance tests (MTT) were performed to evaluate blood glucose, plasma, and insulin. Glucose and lipid oxidation were also assayed during the GTT. At the end of the study, body composition was measured in all the rats, and they were classified as carbohydrate resistant (CR) or carbohydrate sensitive (CS) according to their adiposity. Before sacrifice, 24 of the 48 rats received a calibrated LF/HC meal. Liver, muscle, and intestine tissue samples were taken to measure mRNA expression of key genes involved in glucose, lipid, and protein metabolism. ITT, GTT, and MTT showed that CS rats were neither insulin resistant nor glucose intolerant, but mRNA expression of cholecystokinin (CCK) in the duodenum was higher and that of CPT1, PPARα, and PGC1α in liver were lower than in CR rats. From these results, we make the hypothesis that in CS rats, CCK increased pancreatic secretion, which may favor a quicker absorption of carbohydrates and consequently induces an enhanced inhibition of lipid oxidation in the liver, leading to a progressive accumulation of fat preferentially in visceral deposits. Such a mechanism may explain why CS rats share many characteristics observed in rats fed a high-glycemic index diet.

Low-protein diet-induced hyperphagia and adiposity are modulated through interactions involving thermoregulation, motor activity, and protein quality in mice

Low protein (LP)-containing diets can induce overeating in rodents and possibly in humans in an effort to meet protein requirement, but the effects on energy expenditure (EE) are unclear. The present study evaluated the changes induced by reducing dietary protein from 20% to 6%-using either soy protein or casein-on energy intake, body composition, and EE in mice housed at 22°C or at 30°C (thermal neutrality). LP feeding increased energy intake and adiposity, more in soy-fed than in casein-fed mice, but also increased EE, thus limiting fat accumulation. The increase in EE was due mainly to an increase in spontaneous motor activity related to EE and not to thermoregulation. However, the high cost of thermoregulation at 22°C and the subsequent heat exchanges between nonshivering thermogenesis, motor activity, and feeding induced large differences in adaptation between mice housed at 22°C and at 30°C.