Increased short-term food satiation and sensitivity to cholecystokinin in neurotrophin-4 knock-in mice

Neurotrophin-4 (NT-4) knockout mice exhibited decreased innervation of the small intestine by vagal intraganglionic laminar endings (IGLEs) and reduced food satiation. Recent findings suggested this innervation was increased in NT-4 knock-in (NT-4KI) mice. Therefore, to further investigate the relationship between intestinal IGLEs and satiation, meal patterns were characterized using solid and liquid diets, and cholecystokinin (CCK) effects on 30-min solid diet intake were examined in NT-4KI and wild-type mice. NT-4KI mice consuming the solid diet exhibited reduced meal size, suggesting increased satiation. However, compensation occurred through increased meal frequency, maintaining daily food intake and body weight gain similar to controls. Mutants fed the liquid diet displayed a decrease in intake rate, again implying increased satiation, but meal duration increased, which led to an increase in meal size. This was compensated for by decreased meal frequency, resulting in similar daily food intake and weight gain as controls. Importantly, these alterations in NT-4KI mice were opposite, or different, from those of NT-4 knockout mice, further supporting the hypothesis that they are specific to vagal afferent signaling. CCK suppressed short-term intake in mutants and controls, but the mutants exhibited larger suppressions at lower doses, implying they were more sensitive to CCK. Moreover, devazepide prevented this suppression, indicating this increased sensitivity was mediated by CCK-1 receptors. These results suggest that the NT-4 gene knock-in, probably involving increased intestinal IGLE innervation, altered short-term feeding, in particular by enhancing satiation and sensitivity to CCK, whereas long-term control of daily intake and body weight was unaffected.     

Amino acid supplementation of methanol-grown dried microbial cells in diets for young chicks

Growth rates and efficiency of food conversion of young chicks fed on diets marginally limiting in total nitrogen and containing 150 g/kg diet of flash-dried microbial cells (MC) with and without amino acid supplements, were measured in three experiments. Performance of these animals was compared with that of groups fed on a methioninefortified soya bean meal (SBM) control diet. In all experiments, chicks fed on the SBM control diet grew faster and were more efficient than chicks fed on the basal unsupplemented MC diet. In Experiment 1, arginine supplementation markedly enhanced weight gain and efficiency of food utilisation of chicks offered the basal MC diet; methionine had no effect. The second experiment demonstrated that a supplement containing methionine, arginine and tryptophan was more effective in augmenting the nutritional value of MC than either methionine with arginine or tryptophan with arginine. In the final experiment, weight gain and food intake of chicks fed on MC with supplements of arginine, methionine and tryptophan were increased markedly by additions of lysine and glutamic acid but not by addition of lysine alone. In all experiments, performance of animals in MC supplemented groups was lower than that of animals fed on the SBM control diet.     

Safety assessment of rice genetically modified with soybean glycinin by feeding studies on rats

Feeding studies on rice genetically modified with soybean glycinin were performed on rats for four weeks. The rats were divided into three groups, each being fed on (I) only a commercial diet, (II) this diet plus control rice and (III) this diet plus rice genetically modified with glycinin. The rats were fed with 10 g/kg-weight of rice every day by oral administration. During the test period, the rats in every group grew well without marked differences in appearance, food intake, body weight, or cumulative body weight gain. There were also no significant differences in the blood count, blood composition or internal organ weights among the rats. Necropsy at the end of the experiment indicated neither pathological symptoms nor histopathological abnormalities in the liver and kidney. Judging from these results, the rice genetically modified with glycinin is considered to have been essentially the same in nutritional and biochemical characteristics as the control rice.     

Some New Aryl-5′-fluoro-2′-meth-oxyphenyl Ketones and Their Thiosemicarbazones as Possible Fungicides

Feeding studies on rice genetically modified with soybean glycinin were performed on rats for four weeks. The rats were divided into three groups, each being fed on (I) only a commercial diet, (II) this diet plus control rice and (III) this diet plus rice genetically modified with glycinin. The rats were fed with 10 g/kg-weight of rice every day by oral administration. During the test period, the rats in every group grew well without marked differences in appearance, food intake, body weight, or cumulative body weight gain. There were also no significant differences in the blood count, blood composition or internal organ weights among the rats. Necropsy at the end of the experiment indicated neither pathological symptoms nor histopathological abnormalities in the liver and kidney. Judging from these results, the rice genetically modified with glycinin is considered to have been essentially the same in nutritional and biochemical characteristics as the control rice.     

高比例棉粕饲料中补充蛋氨酸对中华绒螯蟹幼蟹摄食、生长及抗氧化酶活性的影响

以40%棉粕为主的混合蛋白源制成基础饲料, 分别在其中添加0.00%、0.14%、0.28%、0.42%、0.56%蛋氨酸(分别记为0.00%Met、0.14%Met、0.28%Met、0.42%Met和0.56%Met), 配制了5种等氮等能的试验饲料, 以全鱼粉组(64.4%鱼粉)作为对照, 探讨了在高比例棉粕饲料中补充蛋氨酸对中华绒螯蟹幼蟹(0.390.02) g的摄食率、生长率和机体抗氧化酶活性的影响。结果表明: 与全鱼粉对照组相比, 0.42%Met组的增重率、特定生长率和饲料系数均无显著差异(P0.05), 但其显著高于0.00%Met、0.14%Met和0.28%Met组(P0.05); 增重率和特定生长率则显著高于0.56%Met组(P0.05); 从幼蟹的摄食量和蛋白质沉积率来看, 0.42%Met和0.28%Met组的摄食量与对照组相似, 当蛋氨酸的补充量低于0.28%或高于0.42%时, 幼蟹的摄食量均有所下降; 统计表明, 对照组的蛋白质沉积率最高(23.20%), 在各试验组中, 0.28%Met和0.42%Met组之间的蛋白质沉积率无显著差异(P0.05), 但显著高于0.00%Met、0.14%Met和0.56%Met组(P0.05); 分析幼蟹的肠道胰蛋白酶活性, 发现0.42%Met组与对照组之间无显著性差异(P0.05), 但均显著高于其他各试验组(P0.05); 0.28%Met、0.42%Met和0.56%Met处理组的血清丙二醛含量、超氧化物歧化酶活性和谷胱甘肽过氧化物酶活性与对照组无显著差异(P0.05)。结果提示, 在高比例植物蛋白(40%棉粕)的基础饲料中, 补充0.42%Met能够显著提高中华绒螯蟹幼蟹的生长率、消化率和抗氧化酶的活性。       

Effects of a high plant protein diet on the somatotropic system and cholecystokinin in Atlantic salmon (Salmo salar L.)

To investigate the endocrine signalling from dietary plant protein on somatotropic system and gastrointestinal hormone cholecystokinin (CCK), two iso-amino acid diets based on either high plant or high fish meal protein were fed to Atlantic salmon. Salmon with an average starting weight of 641 ± 23 g (N = 180), were fed a fish meal (FM) based diet (containing 40% FM) or diets mainly consisting of blended plant proteins (PP) containing only 13% marine protein, of which only 5% was FM for 3 months. mRNA levels of target genes GH, GH-R, IGF-I, IGF-II, IGFBP-1, IGF-IR in addition to CCK-L, were studied in brain, hepatic tissue and fast muscle, and circulating levels of IGF-I in plasma of Atlantic salmon were measured. We detected reduced feed intake resulting in lower growth, weight gain and muscle protein accretion in salmon fed plant protein compared to a diet based on fish meal. There were no significant effects on the regulation of the target genes in brain or in hepatic tissues, but a trend of down-regulation of IGF-I was detected in fast muscle. Lower feed intake, and therefore lower intake of the indispensable amino acids, may have resulted in lower pituitary GH and lower IGF-I mRNA levels in muscle tissues. This, together with higher protein catabolism, may be the main cause of the reduced growth of salmon fed plant protein diet. There were no signalling effects detected either by the minor differences of the diets on mRNA levels of GH, GH-R, IGF-IR, IGF-II, IGFBP-1, CCK or plasma protein IGF-I.     

Effect of mammalian growth hormone and prolactin on the growth of hypophysectomized chickens

Body weight gain and shank-toe growth during a 26-day treatment period following hypophysectomy were 55 and 46%, respectively, of control values, but the body weight gain was unaffected and bone growth only slightly reduced when the hypophysectomized chickens were fed a low dose of corticosterone (5 ppm). Bovine growth hormone (0.5 mg GH/kg body wt/day for 18 days) enhanced body weight gain and shank-toe length increase (an estimate of bone growth) by 46 and 33%, respectively, compared to the growth of hypophysectomized chickens receiving only corticosterone. These same endpoints were increased approximately 24% after ovine growth hormone treatment in hypophysectomized chickens not receiving corticosterone. Body weight gain during 18 days of treatment with bovine prolactin (0.5 mg PRL/kg/day) was 27% greater than the value for corticosterone-treated hypophysectomized chickens, but bone growth was unaffected. The mammalian GH preparations increased heart weight of the hypophysectomized chickens (25-29%), but pectoralis muscle weight was unaffected. GH treatment enhanced thymal weights by 71% in corticosterone-treated hypophysectomized chickens, and by 93% in hypophysectomized animals not receiving corticosterone. GH had no significant effect on bursal weights, and PRL had no effect on either of these lymphoid organ weights in corticosterone-treated hypophysectomized chickens. GH increased liver and adipose tissue weights considerably more than the large increases that followed treatment of hypophysectomized chickens with corticosterone alone (69 and 126% greater, respectively), but had no effect on these endpoints in hypophysectomized chickens not receiving corticosterone. PRL also greatly increased liver and adipose tissue weights in corticosterone-treated hypophysectomized chickens (79 and 75%, respectively). These results provide evidence that mammalian GH enhances body weight gain, bone growth, and the growth of several organs in the hypophysectomized chicken. Mammalian PRL increased body weight gain, liver weight, and adipose tissue weight in corticosterone-treated hypophysectomized chickens, but did not influence bone growth or the weights of the heart, pectoralis, thymi, or bursa.     

Difructose anhydride III decreases body fat as a low-energy substitute or by decreasing energy intake in non-ovariectomized and ovariectomized female rats

We evaluated the effects of difructose anhydride III (DFAIII) on body weights of ovariectomized rats, which are a good model for obesity by estrogen deficiency-induced overeating. Female rats (10 weeks old) were subjected to ovariectomy or sham operation and then fed with or without a diet containing 3% or 6% DFAIII for 33 days or pair-fed control diet during the same period. Rats fed DFAIII showed significantly decreased food intake, energy intake, body weight gain, body energy accumulation, and fat tissue weight than control group, regardless of ovariectomy. DFAIII may decrease body fat dependent of reduced food/energy intake. Compared with the respective pair feeding groups, rats fed DFAIII showed significantly decreased body energy and fat tissue weight, regardless of ovariectomy, suggesting its potential as a low-energy substitute for high-energy sweeteners. The low energy of DFAIII may contribute to decreased body fat, which may not be dependent on obesity.     

The effect of acarbose on the food intake, weight gain, and adiposity of LA/N-cp rats.

1. Groups of lean and obese LA/N-cp rats were administered the intestinal glucosidase inhibitor acarbose at 150 or 300 mg/kg diet from 7 until 17 weeks of age and the effects of the drug on food intake patterns and adiposity determined. 2. Dose related effects on body weights, adiposity and feed efficiency ratio were observed (control greater than 150 mg greater than 300 mg drug/kg diet) following treatment in both phenotypes, with the greatest differences observed in the obese phenotype. 3. Acarbose at both dosages was associated with phenotype-specific alterations in food intake amount and feeding pattern, resulting in an attenuation of age-associated increases in food intake. The feed efficiency ratio decreased in both phenotypes, and approached normally fed lean controls in obese rats administered the greater dosage. 4. These results indicate that patterns of food intake and weight gain differ markedly between lean and obese rats of this strain, and acarbose brings about a dose-related attenuation of developing food intake patterns in both phenotypes and which are associated with decreases in weight gain and adiposity. Thus, this drug may have therapeutic potential as an adjunct agent in the treatment of obesity and/or other disorders of carbohydrate intolerance.     

House fly larvae meal grown on municipal organic waste as a source of protein in poultry diets

House fly larvae (Musca domestica L.) grown in the residues of municipal organic waste were evaluated as a protein concentrate in practical diets for poultry. Seventy-two broiler-type chicks were alloted within 12 groups. Quadruplicate groups each received the following dietary treatments: a control diet containing soya bean meal alone, or two diets in which either 12% of the supplementary protein was provided by fly larvae meal or 9% by fish meal. The chicks were fed during the first four weeks of life with isocaloric and isoproteic diets and the results showed no significant differences in body weight gain (P > 0.05) or food conversion efficiency (P > 0.05), the larvae meal diet being intermediate to the other two.     

Body growth and substrate partitioning for fat and protein gain in weaned BALB/c mice treated with growth hormone

Previously we have found that recombinant human growth hormone (rhGH) (GH; 74 ng g body wt.(-1)) administration to weaned BALB/c male mice (fed 12% or 20% protein diet) induced a growth lag and subsequent repletion similar to the catch-up growth process. We studied the partitioning of feed and protein intakes between adipose and protein body stores through the linear relationships among them. The non-linear relationship of protein intake with body fat gain/protein gain (FG/PG) ratio was especially adequate in determining the partitioning of substrates. rhGH induced an increase in feed and protein intake utilization for body weight gain (50%) and fat gain (75-140%) over saline; macronutrient utilization was the greatest in rhGH-treated mice fed 20% protein. However, growth recovery of rhGH mice was anomalous and protein intake was derived primarily for fat gain. Mice fed 12% protein (treated and control) also derived protein intake in preference to fat stores. Treatment and diet had a cumulative effect with the result that rhGH-treated animals fed 12% protein showed the greatest FG/PG ratio (1.6), and therefore, the lowest efficiency to gain protein. Weaning is a critical stage in mice when treating with rhGH, as this could provoke a growth lag. The study showed that a high protein level is required to surpass the rhGH-induced lag, but it is not enough to obtain an enhanced protein deposition. Feeding a 12% protein diet was even worse as mice did not improve on the growth lag and substrates were directed mainly to body fat.     

Lipoic acid prevents body weight gain induced by a high fat diet in rats: Effects on intestinal sugar transport

Several studies have suggested that oxidative stress might cause and aggravate the inflammatory state associated with obesity and could be the link between excessive weight gain and its related disorders such as insulin resistance and cardiovascular diseases. Thus, antioxidant treatment has been proposed as a therapy to prevent and manage obesity and associated complications. Therefore, the aim of the present study was to investigate the effects of supplementation of a standard or high fat diet with the antioxidant lipoic acid (LA) during 56 days, on body weight gain, adiposity, feed efficiency and intestinal sugar absorption, in male Wistar rats. LA supplementation induced a lower body weight gain and adipose tissue size in both control or high fat fed rats accompanied by a reduction in food intake. The group fed on a high fat diet and treated with LA (OLIP group) showed a lower body weight gain than its corresponding Pair-Fed (PF) group (P<0.05), which received the same amount of food than LA-treated animals but with no LA. In fact, LA induced a reduction on feed efficiency and also significantly decreased intestinal α-methylglucoside (α-MG) absorption both in lean and obese rats. These results suggest that the beneficial effects of dietary supplementation with LA on body weight gain are mediated, at least in part, by the reduction observed in food intake and feed efficiency. Furthemore, the inhibitory action of LA on intestinal sugar transport could explain in part the lower feed efficiency observed in LA-treated animals and therefore, highlighting the beneficial effects of LA on obesity.     

Lupin as primary protein source in young broiler chicken diets: Effect of enzymes preparations catalyzing degradation of non-starch polysaccharides or phytates

This work examined the effects of three enzyme preparations (A,B,C) directed towards degradation of Non Starch Polysaccharides (NSP) and one targeting phytates (D) on performance traits in broilers fed maize meal basal diets containing 400 g/kg of yellow lupine seeds (LM). A soybean meal (SBM) based diet served as a reference control. Growth rate, coefficients of total tract apparent digestibility (CTTAD) of organic matter, protein and energy, as well as morphometric measurements of selected sections of gastrointestinal tract (GIT) were determined. In comparison to chickens fed the SBM diet, chickens fed the LM diet consumed less feed, had considerably lower body weight gain, as well as lower CTTAD of measured nutrients and energy. Also the GIT relative weight and length were increased within the group fed the LM diet. Addition of each NSP degrading enzymes (A,B,C) to the LM diet increased feed intake and decreased size of GIT organs (all p < 0.05). Addition of enzymes A or B increased (p < 0.05) growth rate of chicks, whereas only enzyme B increased fed efficiency (p < 0.05) and tended to slightly improve CTTAD of nutrients. The addition of enzyme D did not have any effect on feed intake, growth rate or CTTAD. This study indicates that a diet containing high levels of LM is detrimental to feed intake and condition of the digestive tract of young broilers, and thus affects their performance. However, when the LM diet is supplemented with suitable enzyme preparations, performance parameters are not different from those obtained with SBM.     

A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants

Mice deficient in brain-derived neurotrophic factor (BDNF) develop mature-onset obesity, primarily due to overeating. To gain insight into the mechanism of this hyperphagia, we characterized food intake, body weight, meal pattern, and meal microstructure in young and mature mice fed balanced or high-fat diets. Hyperphagia and obesity occurred in mature but not young BDNF mutants fed a balanced diet. This hyperphagia was mediated by increased meal number, which was associated with normal meal size, meal duration, and satiety ratio. In contrast, the high-fat diet induced premature development of hyperphagia and obesity in young BDNF mutants and a similar magnitude hyperphagia in mature mutants. This hyperphagia was supported by increased meal size and was accompanied by a reduced satiety ratio. Thus the mechanism underlying hyperphagia was present before significant weight gain, but whether it occurred, and whether meal frequency or meal size was altered to support it, was modulated by a process associated with aging and by diet properties. Meal pattern changes associated with the balanced diet suggested meal initiation, and the oropharyngeal positive feedback that drives feeding, were enhanced and might have contributed to overeating in BDNF mutants, whereas negative feedback was normal. Consistent with this hypothesis, meal microstructure revealed that all hyperphagic mutant groups exhibited increased intake rates at meal onset. Therefore, the central nervous system targets of BDNF actions may include orosensory brain stem neurons that process and transmit positive feedback or forebrain neurons that modulate its strength.     

Meal-feeding studies in mice: effects of diet on blood lipids and energy expenditure

To identify optimal study-design conditions to investigate lipid metabolism, male, C57BL/6J mice (age, 59 +/- 3 days) were allotted to eight groups, with six animals per group that were stratified by three factors: diet type (high fat [HF]: 60% of energy from fat versus that of a standard rodent diet, 14% fat, fed for 7 weeks), feeding regimen (ad libitum [ad lib] versus meal fed), and metabolic state (data collected in fasted or fed states). Serum free fatty acids (FFA) and triacylglycerols (TAG) concentrations, and energy expenditure (EE) were assessed. Mice gained 0.30 +/- 0.11 g of body weight/day when allowed ad lib access to HF diet, similar weight when meal-fed the HF or ad lib-fed the standard diet (0.10 +/- 0.03 g/day), and no weight when meal-fed the standard diet (0.01 +/- 0.02 g/day). Fed-state TAG concentration was 88 to 100% higher (P < 0.02) than that of the fasted state, except when animals were ad lib-fed the HF diet. When the standard diet was meal fed, FFA concentration was 30% higher in the fasted compared with the fed state (P = 0.003). Mice had 33% higher postprandial EE when either diet was meal fed (P = 0.01). Mice adapted to meal feeding developed transitions in metabolism consistent with known physiologic changes that occur from fasting to feeding. When fed the standard diet, a 6-h per day meal-feeding regimen was restrictive for normal growth. These data support use of a meal-feeding regimen when HF diets are used and research is focused on metabolic differences between fasted and fed states. This protocol allows study of the metabolic effects of an HF diet without the confounding effects of over-consumption of food and excess body weight gain.     

Food restriction and refeeding in growing rats.

1. The interrelationship between food intake, body weight and oxygen consumption was analysed at 25 degrees C in growing rats. 3. The experiment was divided into two phases lasting four weeks each. During the first phase the animals were subjected to energy restriction and during the second phase they were allowed ad lib energy intake. Four groups of rats were studied: Control with ad lib food intake and three restricted groups R4, R5, and R6 which received during the first phase 4, 5, and 6 g per day of stock diet in a single meal. 3. The results showed a decrease in body weight and oxygen consumption during the restriction period and a recovering of the latter during the refeeding period, without body weight recovering. 4. It is concluded that an energy conservation mechanism is present during food restriction and for some time after refeeding.     

Changes in enzymatic activity of small intestine and kidney of rats by a methionine deficient diet

The effect of methionine dietary deficiency on food intake, weight gain, liver and kidney weight, feed conversion rate, protein efficiency ratio, maltase and leucineaminopeptidase (LAPase) activities of the intestinal mucosa as well as renal LAPase activity was studied. Three groups of female Wistar rats, weighing between 40-60 g, were fed for 25 days on either Diet A (casein supplemented with 0.6% DL-methionine), Diet B (amino acid mixture simulating casein also supplemented with 0.6% methionine) or Diet C (amino acid mixture with 0.67% methionine deficiency with respect to Diet A). The results show no significant differences in either growth or enzymatic activity between the rats fed on Diet A and those on Diet B. The animals fed on Diet C show an increase in intestinal (P less than 0.01, vs Diet B) and renal (P less than 0.005, vs Diet A) LAPase activity, although intestinal maltase activity remained unchanged. Food intake, weight gain, organ weight and nutritional parameters obtained in rats fed on Diet C showed no statistically significant changes, with the exception of kidney weight which decreased (P less than 0.005) when compared to those fed on Diet B.     

Dietary whey protein decreases food intake and body fat in rats

We investigated the effects of dietary whey protein on food intake, body fat, and body weight gain in rats. Adult (11-12 week) male Sprague-Dawley rats were divided into three dietary treatment groups for a 10-week study: control. Whey protein (HP-W), or high-protein content control (HP-S). Albumin was used as the basic protein source for all three diets. HP-W and HP-S diets contained an additional 24% (wt/wt) whey or isoflavone-free soy protein, respectively. Food intake, body weight, body fat, respiratory quotient (RQ), plasma cholecystokinin (CCK), glucagon like peptide-1 (GLP-1), peptide YY (PYY), and leptin were measured during and/or at the end of the study. The results showed that body fat and body weight gain were lower (P < 0.05) at the end of study in rats fed HP-W or HP-S vs. control diet. The cumulative food intake measured over the 10-week study period was lower in the HP-W vs. control and HP-S groups (P < 0.01). Further, HP-W fed rats exhibited lower N(2) free RQ values than did control and HP-S groups (P < 0.01). Plasma concentrations of total GLP-1 were higher in HP-W and HP-S vs. control group (P < 0.05), whereas plasma CCK, PYY, and leptin did not differ among the three groups. In conclusion, although dietary HP-W and HP-S each decrease body fat accumulation and body weight gain, the mechanism(s) involved appear to be different. HP-S fed rats exhibit increased fat oxidation, whereas HP-W fed rats show decreased food intake and increased fat oxidation, which may contribute to the effects of whey protein on body fat.     

A putative physiological role of hypothalamic CNTF in the control of energy homeostasis

Administration of CNTF durably reduces food intake and body weight in obese humans and rodent models. However, the involvement of endogenous CNTF in the central regulation of energy homeostasis needs to be elucidated. Here, we demonstrate that CNTF and its receptor are expressed in the arcuate nucleus, a key hypothalamic region controlling food intake, and that CNTF levels are inversely correlated to body weight in rats fed a high-sucrose diet. Thus endogenous CNTF may act, in some individuals, as a protective factor against weight gain during hypercaloric diet and could account for individual differences in the susceptibility to obesity.