Dietary Weight Gain Research Articles

Interaction of Wheat Bran Particle Size and Stimbiotic Supplementation on Growth Performance and Gut Health Parameters in Broilers.

A 42-day study was conducted with 720-day-old Cobb male broiler chicks allocated to treatments in a 3 × 2 factorial, with the factors as wheat bran (WB) inclusion (no WB, 50 g/kg coarse WB, or 50 g/kg fine WB) and stimbiotic (STB) supplementation in corn-based diets. The inclusion of WB (p < 0.05) or STB supplementation (p < 0.05) increased the FCR and feed intake in the day 0-10 phase. During the day 0-28 phase, coarse-WB inclusion increased (p < 0.05) the FCR, compared to fine WB or diets without WB. In the day 0-42 phase, WB marginally decreased weight gain in diets without STB supplementation, but the STB-supplemented diet, weight gain was greater (p < 0.05) the diet with fine WB compared with diets with coarse WB. Fine-WB inclusion increased the ileal nitrogen and energy digestibility determined at day 18 compared to coarse WB or diets without WB. Supplementation with STB (p < 0.05) or fine WB (p < 0.05) inclusion increased the villi height compared to diets without STB supplementation or coarse WB, or the diet without WB. Coarse or fine WB decreased (p < 0.05) cecal branched-chain fatty acids compared to diets without WB. In conclusion, stimbiotic supplementation to fine WB improved the performance and nutrient digestibility of broilers compared to coarse WB with no effects on the caeca total SCFA concentration.

ABHD11, a new diacylglycerol lipase involved in weight gain regulation.

Obesity epidemic continues to spread and obesity rates are increasing in the world. In addition to public health effort to reduce obesity, there is a need to better understand the underlying biology to enable more effective treatment and the discovery of new pharmacological agents. Abhydrolase domain-containing protein 11 (ABHD11) is a serine hydrolase enzyme, localized in mitochondria, that can synthesize the endocannabinoid 2-arachidonoyl glycerol (2AG) in vitro. In vivo preclinical studies demonstrated that knock-out ABHD11 mice have a similar 2AG level as WT mice and exhibit a lean metabolic phenotype. Such mice resist to weight gain in Diet Induced Obesity studies (DIO) and display normal biochemical plasma parameters. Metabolic and transcriptomic analyses on serum and tissues of ABHD11 KO mice from DIO studies show a modulation in bile salts associated with reduced fat intestinal absorption. These data suggest that modulating ABHD11 signaling pathway could be of therapeutic value for the treatment of metabolic disorders.

Obesity-induced reduction of adipose eosinophils is reversed with low-calorie dietary intervention.

While many studies have characterized the inflammatory disposition of adipose tissue (AT) during obesity, far fewer have dissected how such inflammation resolves during the process of physiological weight loss. In addition, new immune cells, such as the eosinophil, have been discovered as part of the AT immune cell repertoire. We have therefore characterized how AT eosinophils, associated eosinophilic inflammation, and remodeling processes, fluctuate during a dietary intervention in obese mice. Similar to previous reports, we found that obesity induced by high‐fat diet feeding reduced the AT eosinophil content. However, upon switching obese mice to a low fat diet, AT eosinophils were restored to lean levels as mice reached the body weight of controls. The rise in AT eosinophils during dietary weight loss was accompanied by reduced macrophage content and inflammatory expression, upregulated tissue remodeling factors, and a more uniformly distributed AT vascular network. Additionally, we show that eosinophils of another metabolically relevant tissue, the liver, did not oscillate with either dietary weight gain or weight loss. This study shows that eosinophil content is differentially regulated among tissues during the onset and resolution of obesity. Furthermore, AT eosinophils correlated with AT remodeling processes during weight loss and thus may play a role in reestablishing AT homeostasis.

Effect of cereal type and Xylanase supplementation on nutrient retention and growth performance of broilers

An experiment was conducted to study the effect of cereal (corn, wheat, barley and sorghum) and supplemental enzyme (a mono-component xylanase) in a 4 × 2 factorial arrangement. A 2-phase feeding program (0 to 21 and 21 to 42 d) was used and 4 iso-caloric, iso-nitrogenous diets were formulated containing corn, wheat, barley, or sorghum as the sole cereal. Diets based on each cereal were fed without or with supplemental xylanase (16,000 BXU/kg) to 8 replicate pens of 10 chicks (5 male : 5 female, Cobb 500) each. Growth performance was recorded at 21 or 42 d posthatch. Excreta was quantitatively collected from 18 to 21 and 38 to 41 d for the measurement of the total tract retention of dry matter (DM), nitrogen (N) and neutral detergent fiber (NDF) and apparent metabolizable energy (AME). Ileal digestible energy (IDE) was measured at the end of the study (42 d posthatch) using titanium dioxide as an indigestible marker. For the overall 42 d period, birds fed barley-based diets had lower feed intake (P < 0.05), lower body weight (P < 0.05) and converted feed into gain less efficiently (P < 0.05) compared with the diets based on corn, wheat or sorghum. Xylanase supplementation improved weight gain in diets based on corn, wheat, and sorghum with the exception of barley-based diets (cereal × xylanase interaction, P < 0.05). Xylanase improved the overall feed conversion ratio (1.885 vs. 1.939; P < 0.05) with the effect being independent of the cereal type. The N retention of barley-based diets was lower (P < 0.05) compared with the other cereals, while xylanase improved N retention (P < 0.05) regardless of the cereal type. NDF digestibility differed (P < 0.05) across cereal (barley > wheat > corn > sorghum) and was improved (P < 0.05) by xylanase supplementation. A significant cereal × xylanase interaction (P < 0.05) was observed for energy measurements, where xylanase improved IDE of the corn-based diet, and AME of corn- and wheat-based diets. Results of the current study demonstrate potential of xylanase in improving nutrient retention and growth performance of broilers fed diets based on variety of cereal grains.

The influence of meat-and-bone meal and exogenous phytase on growth performance, bone mineralisation and digestibility coefficients of protein (N), amino acids and starch in broiler chickens.

The objective of this study was to examine the influence of meat-and-bone meal (MBM) and phytase inclusion on growth performance, bone mineralisation and apparent digestibility coefficients of nutrients in broiler chickens offered wheat-based diets. The feeding study comprised 7 dietary treatments: positive control (PC, 9.0% Ca and 4.5% available phosphorous [AvP] in starter, 7.0% Ca and 3.5% AvP in finisher); negative control (NC, 7.2% Ca and 3.0% AvP in starter, 5.2% Ca and 2.0% AvP in finisher) diets incorporating a 3 × 2 factorial array of 3 MBM inclusions (0, 60, 120 g/kg) and 2 levels of phytase supplementation (0 and 1,000 FYT/kg). Each treatment was allocated to 6 replicated pens with 30 birds per pen in an environmentally-controlled deep litter facility. A total of 1,260 one-day-old male Ross 308 chicks were offered starter diets from 1 to 14 days post-hatch and finisher diets from 15 to 36 days post-hatch. There were significant (P < 0.05) interactions between MBM inclusions and phytase supplementation on weight gain and feed intake in starter diets. Phytase significantly increased weight gain in diets without MBM and did not influence weight gain in diets with 60 and 120 g/kg MBM. Collectively, increasing MBM inclusion significantly reduced weight gain in starter diets (P < 0.0001). There were dietary interactions (P < 0.01) on toe ash where phytase significantly improved toe ash in diet without MBM and did not influence toe ash in the other two groups of negative control diets. There were no dietary treatment interactions on apparent ileal digestibility coefficients of starch and protein except that diets without MBM had significantly (P < 0.01) lower ileal starch digestibility and diets with 120 g/kg MBM had significantly (P < 0.0001) lower ileal protein digestibility. No dietary influence on ileal fat digestibility was observed. There were dietary interactions on ileal digestibilities of isoleucine, valine and glycine. Phytase significantly increased glycine digestibility in diets with 60 and 120 g/kg MBM but not in diets without MBM. Including 120 g/kg MBM significantly (P < 0.01) depressed apparent digestibility coefficients of 13 ex 16 amino acids in the distal ileum. This study demonstrated the negative impacts of MBM on amino acid digestibility and growth performance. Also, responses to phytase were more pronounced in diets without MBM, which may have been due to their relatively lower available P and higher phytate concentrations in comparison to diets containing MBM.

Changes in fatty acid profiles of sea cucumber Apostichopus japonicus (Selenka) induced by terrestrial plants in diets

It has been well known that fatty acid profiles of consumers were flexible in response to the changes in the fatty acid constituents of diets due to the different feed ingredients. No previous studies, however, have been carried out focused on the changes in fatty acid profiles of sea cucumber Apostichopus japonicus (Selenka) induced by the addition of terrestrial plants in diets. In the present study, 4 experimental diets were prepared with gradually increased proportions of terrestrial plants (corn meal and soybean meal) and concurrently decreased proportions of seaweed Sargassum thunbergii. The artificial feed of sea cucumber containing 50% of S. thunbergii was used as the control diet (diet 1), and S. thunbergii were replaced by the mixture of corn meal and soybean meal with the percentages of 10%, 20% and 30% in diets 2, 3 and 4, respectively. Fatty acid profiles of feed ingredients and sea cucumbers fed with the 4 experimental diets were determined. Results showed that fatty acid compositions of sea cucumbers were remarkably affected by those of the diets. Concentrations of fatty acids 16:0, 18:2n-6, 22:6n-3 and ∑ n-6 in sea cucumbers appeared to positively correlate with those in the diets. In contrast, contents of fatty acids 20:1n-9, 22:1n-9, 20:3n-3, 20:4n-6 and 20:5n-3 in sea cucumbers showed a significant increase with the increasing levels of corn meal and soybean meal in diets, even though the contents of these fatty acids in corn meal and soybean meal were lower, even absent, compared with S. thunbergii suggesting that sea cucumbers might have the ability to synthesize these fatty acids. Data of the growth performance revealed that sea cucumbers showed the highest weight gain in diet 2 and the lowest weight gain in diet 4 while the growth of the sea cucumbers in diet 3 did not remarkably differ with those in the control group.

AT1 receptor blockade alters nutritional and biometric development in obesity-resistant and obesity-prone rats submitted to a high fat diet.

Obesity is a chronic metabolic condition with important public health implications associated with numerous co-morbidities including cardiovascular disease, insulin resistance, and hypertension. The renin angiotensin system (RAS), best known for its involvement in cardiovascular control and body fluid homeostasis has, more recently, been implicated in regulation of energy balance. Interference with the RAS (genetically or pharmacologically) has been shown to influence body weight gain. In this study we investigated the effects of systemic AT1 receptor blockade using losartan on ingestive behaviors and weight gain in diet induced obese (DIO) rats. Prior to losartan administration (30 mg/kg/day) body weight gain remained constant within the DIO animals (3.6 ± 0.3 g/day, n = 8), diet resistant (DR) animals (2.1 ± 0.6 g/day, n = 8) and in the age-matched chow fed control (CHOW) animals (2.8 ± 0.3 g/day, n = 8), Losartan administration abolished body weight gain in animals fed a high fat diet (DIO: -0.4 ± 0.7 g/day, n = 8; and DR: -0.8 ± 0.3 g/day, n = 8) while chow fed animals continued to gain weight (2.2 ± 0.3 g/day, n = 8) as they had previously to oral administration of losartan. This decrease in daily body weight gain was accompanied by a decrease in food intake in the HFD fed animals. Following the removal of losartan, both the DIO and DR animals again showed daily increases in body weight gain and food intake which were similar to control values. Our data demonstrate that oral losartan administration attenuates body weight gain in animals fed a HFD whether the animal is obese (DIO) or not DR while having no effect on body weight gain in age-matched chow fed animals suggesting a protective effect of losartan against body weight gain while on a HFD.

Lymphotoxin reduces commensal diversity to enable diet induced obesity (120.2)

Abstract Commensal microbes exist in a state of symbiosis with host immunity and are essential for weight gain in diet induced obesity (DIO). Lymphotoxin α (LTα), a key molecule in mucosal defense, has been linked to obesity. We report that mice lacking LTα, LTβ, and LTβ-receptor (LTβR) resist DIO. The microbial communities of LTβR+/- mice and LTβR-/- mice differed on normal chow (NCD) and after high fat diet (HFD). The microbial community of LTβR+/- mice was less diverse after HFD, a hallmark of the “obese microbiome” in humans. On the contrary, LTβR-/- animals maintained similarly diverse communities to their NCD counterparts while on HFD. A specific microbe, Segmented Filamentous Bacteria (SFB), was cleared after HFD in LTβR+/- but not LTβR-/- mice and served as a marker of diversity loss. Transplantation of cecal contents from LTβR-/- animals conferred less weight gain than that of LTβR+/- mice to WT germ free mice, demonstrating a causal relationship between differing microbiota and weight gain. Housing LTβR-/- mice with their LTβR+/- siblings rescued weight gain, demonstrating horizontal transmissibility of the obese phenotype. HFD induced IL-23, an SFB associated cytokine, within the colon, but this induction was absent in LTβR-/- mice. Mice deficient in IL-23 (p19-/-) and the downstream cytokine IL-22 (RORγt-/-) also resisted DIO. Our data suggests that HFD induced inflammation reduces commensal diversity to enable weight gain, which may underlie the pathogenesis of obesity.

Losartan prevents body weight gain in diet induced obese rats

The renin angiotensin system (RAS), best known for its involvement in the regulation of cardiovascular function and salt/water balance, has recently been suggested to play a role in the regulation of energy homeostasis as interference with systemic RAS activity has been shown to decrease body weight and fat. The present study was undertaken to determine whether losartan, a non‐peptide ATII Type 1 receptor blocker, would influence daily body weight gain in diet induced obese (DIO) rats.Male Sprague Dawley rats (125–150g) were exposed to either a HFD or fed standard rat chow. After 10 weeks, rats on HFD were divided into DIO or diet resistant (DR) and at 18 weeks, body weight, and food and water intake were measured daily for 5 weeks. After a 14 day control period, rats were administered losartan (30mg/kg) in drinking water for 14 days, followed by return to tap water for an additional 7 days and effects on body weight and food and water intake assessed.There was no difference in daily body weight gain during in the control period between chow fed (2.6±0.5g, n=8), DR (2.1±0.5g, n=8) or DIO rats (3.4±0.4g, n=8, p=.18, one way ANOVA). Although losartan treatment attenuated daily body weight gain in chow fed rats (1.25±0.5g, n=8), it completely abolished daily weight gain in DR (−0.65±0.3g, n=8) and DIO (−0.43±0.7g, n=8) rats. Upon return to normal tap water, all rats gained weight as they had prior to losartan administration (chow 3.3±0.2g, DR 2.9±0.5g, DIO 3.8±0.5g).Our data demonstrate that losartan attenuates body weight gain in rats fed either a HFD (DR and DIO) or chow diet, an effect which was more pronounced in animals fed the HFD. These data suggest that the RAS plays a role in body weight homeostasis and that pharmacological agents that interfere with the functioning of the RAS may have be useful in the treatment for obesity.

Intake and digestibility of concentrate and legume hay diets fed to foals

This study was carried out to evaluate intake, nutrient digestibility and body weight gain of foals on diets of concentrate and legume hay. Treatments were: lucerne hay (Medicago sativa), Campo Grande stylo hay (20% Stylosanthes macrocephala and 80% Stylosanthes capitata) and Mineirão stylo hay (Stylosanthes guianensis cv. Mineirão). Fifteen weaned foals at 160 Kg body weight (BW) were used. The experiment was entirely randomized with three treatments and five replicates. Dry matter intake was estimated at 30 g of dry matter (DM)/kg BW and was comprised of 40% concentrate meal and 60% hay. Fecal production and nutrient digestibility were calculated by the LIPE® marker methodology. There was no difference between Lucerne hay and Campo Grande stylo hay intake, but intake of Mineirão stylo hay was lower than that of Lucerne hay. Body weight gain and nutrient digestibility coefficients were similar for foals fed different diets. Intake was similar for Campo Grande and Lucerne hay, and led to similar body weight gain in diets with concentrate. Mineirão stylo hay, at 137 days of growth, was not palatable for the foals.

Discovery of Orally Active Carboxylic Acid Derivatives of 2-Phenyl-5-trifluoromethyloxazole-4-carboxamide as Potent Diacylglycerol Acyltransferase-1 Inhibitors for the Potential Treatment of Obesity and Diabetes

Diacylglycerol acyltransferase-1 (DGAT-1) is the enzyme that catalyzes the final and committed step of triglyceride formation, namely, the acylation of diacylglycerol with acyl coenzyme A. DGAT-1 deficient mice demonstrate resistance to weight gain on high fat diet, improved insulin sensitivity, and reduced liver triglyceride content. Inhibition of DGAT-1 thus represents a potential novel approach for the treatment of obesity, dyslipidemia, and metabolic syndrome. In this communication, we report the identification of the lead structure 6 and our lead optimization efforts culminating in the discovery of potent, selective, and orally efficacious carboxylic acid derivatives of 2-phenyl-5-trifluoromethyloxazole-4-carboxamides. In particular, compound 29 (DGAT-1 enzyme assay, IC(50) = 57 nM; CHO-K1 cell triglyceride formation assay, EC(50) = 0.5 μM) demonstrated dose dependent inhibition of weight gain in diet induced obese (DIO) rats (0.3, 1, and 3 mg/kg, p.o., qd) during a 21-day efficacy study. Furthermore, compound 29 demonstrated improved glucose tolerance determined by an oral glucose tolerance test (OGTT).

The Act of Voluntary Wheel Running Reverses Dietary Hyperphagia and Increases Leptin Signaling in Ventral Tegmental Area of Aged Obese Rats

To test the hypothesis that exercise increases central leptin signaling, and thus reduces dietary weight gain in an aged obese model, we assessed the effects of voluntary wheel running (WR) in 23-month-old F344×BN rats fed a 60% high-fat (HF) diet for 3 months. After 2 months on the HF diet, half of the rats were provided access to running wheels for 2 weeks while the other half remained sedentary. Following the removal of the wheels, physical performance was evaluated, and 4 weeks later leptin signaling was assessed in hypothalamus and VTA after an acute bout of WR. Introduction of a HF diet led to prolonged hyperphagia (63.9 ± 7.8 kcal/day on chow diet vs. 88.1 ± 8.2 kcal/day on high-fat diet (when food intake stabilized), p < 0.001). As little as 9 (ranging to 135) wheel revolutions per day significantly reduced caloric consumption of HF food (46.8 ± 11.2 kcal/day) to a level below that on chow diet (63.9 ± 7.8 kcal/day, p < 0.001). After 2 weeks of WR, body weight was significantly reduced (7.9 ± 2.1% compared with prerunning weight, p < 0.001), and physical performance (latency to fall from an incline plane) was significantly improved (p = 0.04). WR significantly increased both basal (p = 0.04) and leptin-stimulated (p = 0.001) STAT3 phosphorylation in the ventral tegmental area (VTA), but not in the hypothalamus. Thus, in aged dietary obese rats, the act but not the extent of voluntary WR is highly effective in reversing HF consumption, decreasing body weight, and improving physical performance. It appears to trigger a response that substitutes for the reward of highly palatable food that may be mediated by increased leptin signaling in the VTA.

Effects of different diets on weight gain,hepatic lipase and antioxidant enzyme of juvenile silver pomfret(&lt;I&gt;Pampus argenteus&lt;/I&gt;)

A 9-week feeding experiment was carried out on juvenile silver pomfret Pampus argenteus[initial weight,(4.80±0.11) g]to evaluate the effects of feed composition on weight gain,feed conversion ratio(FCR),hepatic lipase and antioxidant enzyme activities using nutriology and biochemistry.Four diets were formulated and named diet 1(fresh fish meat),diet 2(fresh fish meat mixed with formulated feed),diet 3(fresh fish meat mixed with formulated feed and solen meat) and diet 4(fresh fish meat mixed with formulated feed,solen meat and copepods).Each diet was assigned to triplicate groups.The results showed that the weight gain of silver pomfret could be affected significantly by the feed composition.The weight gain of diet 1 was the lowest among the four diets,and was significantly lower than those of other three diets.The weight gain of diet 4 was the highest,and was significantly higher than those of diet 2 and diet 3(P0.05).The FCR of diet 1 was the highest among the four diets,and was significantly higher than those of other three diets.There was no significant difference in FCR among diet 2,diet 3 and diet 4(P0.05).Hepatic lipase and total lipase activities of diet 1 were significantly lower than those of other diets(P0.05),but no significant difference was found in hepatic lipase,lipoprotein lipase and total lipase activities among diet 2,diet 3 and diet 4(P0.05).There was no significant difference in superoxide dismutase(SOD) and glutathione peroxidase(GSH-PX) activities among all diets(P0.05).However,the lowest SOD and GSH-PX activities were both in diet 1 and highest were in diet 4.The catalase(CAT) activity of diet 4 was significantly higher than those of diet 1,2 and 3(P0.05),but no significant difference was found among diet 1,2 and 3(P0.05).In conclusion,the only use of fish meat as a feed is not beneficial to the growth of silver pomfret.Copepods could be also used in the diet to improve the growth and antioxidant ability of silver pomfret.

Leptin resistance: a prediposing factor for diet-induced obesity

Obesity is a resilient and complex chronic disease. One potential causative factor in the obesity syndrome is leptin resistance. Leptin behaves as a potent anorexic and energy-enhancing hormone in most young or lean animals, but its effects are diminished or lacking in the obese state associated with a normal genetic background. Emerging evidence suggests that leptin resistance predisposes the animal to exacerbated diet-induced obesity (DIO). Elevation of central leptin in young, lean rats induces a leptin resistance that precludes obesity on a chow diet but accelerates high-fat (HF)-induced obesity. Similarly, chronic dietary fructose consumption evokes a leptin resistance that causes obesity only upon HF exposure. Inherent central leptin insensitivity also contributes to dietary weight gain in certain obesity-prone rats. Conversely, aged, leptin-resistant animals are obese with continuous chow feeding and demonstrate aggravated obesity when challenged with an HF diet. Additionally, a submaximal central blockade with a leptin antagonist leads to obesity on both chow and HF diets, as is the case in rodents with leptin receptor deficiency of genetic origin. Despite the differences in the incidence of obesity on a chow diet, all of these forms of leptin resistance predispose rodents to aggravated HF-mediated obesity. Moreover, once leptin resistance takes hold, it aggravates DIO, and the leptin resistance and obesity compound one another, promoting a vicious cycle of escalating weight gain.

Synergy Between Leptin Therapy and a Seemingly Negligible Amount of Voluntary Wheel Running Prevents Progression of Dietary Obesity in Leptin-Resistant Rats

We examined whether chronic leptin treatment of diet-induced obese rats promotes or alleviates the susceptibility to continued high-fat feeding. Second, we examined if voluntary wheel running is beneficial in reducing the trajectory of weight gain in high-fat-raised leptin-resistant rats. Sprague-Dawley rats were fed a standard diet or a high-fat diet for 5 months, and then hypothalamic leptin overexpression was induced through central administration of adeno-associated virus-encoding leptin while continuing either the standard or high-fat diet. Two weeks later, half of the rats in each group were provided access to running wheels for 38 days while being maintained on either a standard or high-fat diet. RESULTS; In standard diet-raised rats, either wheel running or leptin reduced the trajectory of weight gain, and the combined effect of both treatments was additive. In high-fat-raised leptin-resistant rats, leptin overexpression first transiently reduced weight gain but then accelerated the weight gain twofold over controls. Wheel running in high-fat-raised rats was sixfold less than in standard diet-raised rats and did not affect weight gain. Surprisingly, wheel running plus leptin completely prevented weight gain. This synergy was associated with enhanced hypothalamic signal transducer and activator of transcription (STAT) 3 phosphorylation and suppressor of cytokine signaling 3 expression in wheel running plus leptin compared with leptin-treated sedentary high-fat counterparts. This enhanced STAT3 signaling associated with the combination treatment occurred only in high-fat-raised, leptin-resistant rats and not in standard diet-raised, leptin-responsive rats. Chronic leptin treatment in diet-induced obese rats accelerates dietary obesity. However, leptin combined with wheel running prevents further dietary weight gain. Thus, this combination therapy may be a viable antiobesity treatment.

Role of the Duodenum and Macronutrient Type in Ghrelin Regulation

The orexigenic hormone ghrelin is implicated in preprandial hunger and meal initiation in part because circulating levels increase before meals and decrease after food intake. The mechanisms underlying postprandial ghrelin suppression are unknown. Although most ghrelin is produced by the stomach, we have shown that neither gastric nutrients nor gastric distension affect ghrelin levels. We hypothesized that the nutrient-sensing mechanism regulating ghrelin is in the duodenum, the second richest source of ghrelin. To test whether duodenal nutrient exposure is required for ghrelin suppression, we infused nutrients into either the proximal duodenum or proximal jejunum in rats bearing chronic intestinal cannulas. At 0, 30, 60, 90, 120, 180, 240, and 300 min after infusions, blood was sampled via jugular-vein catheters for ghrelin, insulin, and glucose measurements. To elucidate further the mechanisms governing nutrient-related ghrelin suppression, we also assessed the ghrelin responses to isocaloric (3 kcal) infusions of glucose, amino acids, or lipids delivered into the stomach or small intestine of chronically catheterized rats. Regardless of macronutrient type, the depth and duration of ghrelin suppression were equivalent after gastric, duodenal, and jejunal infusions. Glucose and amino acids suppressed ghrelin more rapidly and strongly (by approximately 70%) than did lipids (by approximately 50%). Because jejunal nutrient infusions suppressed ghrelin levels as well as either gastric or duodenal infusions, we conclude that the inhibitory signals mediating postprandial ghrelin suppression are not derived discretely from either the stomach or duodenum. The relatively weak suppression of ghrelin by lipids compared with glucose or amino acids could represent one mechanism promoting high-fat dietary weight gain.

Dephytinization of two soy proteins increases phosphorus and protein utilization by rainbow trout, Oncorhynchus mykiss

The efficacy of pre-treating two soy proteins with phytase (dephytinization) was evaluated in 2×3 factorial trial with rainbow trout [two soy proteins, three treatments (no treatment, dephytinization, P supplement)]. Two commercial soy proteins, Soycomil P and Hamlet Protein 300, were fed with no supplemental phosphorus (P), or with 3 g supplemental P kg −1 diet. Experimental dephytinized batches of the soy proteins were prepared by wet incubation with microbial phytase (BASF Natuphos) and included in diets without supplemental P. The soy product contents were 600 g kg −1 diets. P contents were 6–9 g kg −1 in diets with and without supplemental P, respectively. Initially, 57-g fish were fed in triplicate tanks for 9 weeks. Dephytinization had a positive effect on weight gain, feed efficiency and on protein, P, calcium, magnesium and zinc utilization. Weight gain was better in fish fed dephytinized soy proteins than in fish fed untreated regular soy fortified with P. P retention averaged 33% in fish fed regular soy proteins and 72% in fish fed dephytinized soy protein. P load into the water from fish fed diets with 60% dephytinized soy proteins averaged 1.5 g P kg −1 weight gain, compared to 4.3 g P kg −1 weight gain in diets with untreated soy proteins. Although similarly low P loads cannot yet be expected from practical diets, dephytinization of soy with phytase could offer a powerful tool for nutrient discharge management in aquaculture.