Dietary Β-conglycinin Research Articles

Dietary β-Conglycinin Combined with Exercise Synergistically Induces Beige Adipocyte Formation in Association with Fibroblast Growth Factor 21 Production in Mice

Dietary β-Conglycinin Combined with Exercise Synergistically Induces Beige Adipocyte Formation in Association with Fibroblast Growth Factor 21 Production in Mice

Dietary high β-conglycinin reduces the growth through enhancing hepatic lipid peroxidation and impairing intestinal barrier function of orange-spotted grouper (Epinephelus coioides)

β-conglycinin is one of the major soy antigen proteins in soybean meal (SBM) and exhibits growth inhibition and intestinal health damage in grouper, but the underlying mechanisms are still poorly understood. In this study, orange-spotted grouper (Epinephelus coioides) was used to investigate whether the poor growth performance induced by dietary β-conglycinin levels is associated with intestinal structural integrity disruption, the intestinal apoptosis and intestinal microbiota. The basal diet (FM diet) was formulated to contained 48% protein and 12% fat without SBM supplementation. Fish meal protein in the FM diet was replaced by SBM to prepare a high SBM diet (SBM diet). β-conglycinin at 3% and 7% were added into FM diets to prepare two diets (B-3 and B-7). Triplicate groups of fish (20 fish/tank) were fed one of the experimental diets twice daily in a feeding period of 8 weeks. Compared with FM diet, fish fed diets SBM and B-7 had decreased the growth rate, hepatosomatic index, whole-body lipid and ash contents, and increased whole-body moisture content. However, the maximum growth was observed for diet B-3 and was not different from that of FM diet. The liver total antioxidant capacity and glutathione peroxidase activity, the muscle layer thickness of middle and distal intestine, and the mucosal fold length of distal intestine were lower, while liver malondialdehyde content, intestinal diamine oxidase activity, d-lactic acid and endotoxin contents, and the number of intestinal apoptosis were higher in SBM and B-7 groups than that in FM and/or B-3 groups. SBM and B-7 diets down-regulated the intestinal expression of tight junction genes (occludin, claudin-3 and ZO-1), apoptosis genes (bcl-2 and bcl-xL) and anti-inflammatory factor genes (IκBα, TGF-β1 and IL-10), but up-regulated the intestinal expression of apoptosis genes (caspase-3, caspase-8 and caspase-9) and pro-inflammatory factor genes (NF-κB1, RelA, TAK1, IKK, MyD88, TNF-α, IL-1β, and IL-8) vs FM and/or B-3 diets. The richness and diversity indexes of OTUs, Chao1, ACE, Shannon and Simpson were not affected by dietary treatments. The relative abundances of intestinal bacteria (phylum Proteobacteria and genus Vibrio) were generally higher, and relative abundance of phylum Tenericutes was lower in SBM and/or B-7 groups than that in B-3 group. The above results indicate that high dietary β-conglycinin level, rather than intermediate level could decrease liver antioxidant capacity, reshape the intestinal microbiota, and impair the intestinal normal morphology through disrupting the intestinal tight junction structure, increasing intestinal mucosal permeability, and promoting intestinal apoptosis, which in turn triggers intestinal inflammatory responses and the occurrence of enteritis, and ultimately leads to poor growth performance in fish.

Dietary β-conglycinin induces intestinal enteritis and affects glycerophospholipid and arginine metabolism in mirror carp (Cyprinus carpio)

The use of soybean meal in aquafeed industry is partially limited by anti-nutritional factors such as β-conglycinin (β-CG). However, the effects of β-CG on mirror carp (Cyprinus carpio) growth performance and intestinal health has not been elucidated. This study investigated the effects of β-CG levels on growth performance, intestine immunity, and intestinal lipid and protein metabolism in mirror carp. Four hundred and fifty mirror carp (4.22 ± 0.03) g were fed a control (CON) diet containing fish meal as the protein source and four experimental diets containing β-CG at 40 (β-CG1), 80 (β-CG2), 120 (β-CG3), and 160 g/kg (β-CG4) replacing the fishmeal, respectively. Each treatment had 30 fish replicated three times and the feeding was done for six weeks. The results showed that weight gain, specific growth rate, survival rate, protein efficiency, feed conversion ratio, and condition factor were not affected by dietary β-CG (P > 0.05). Interestingly, the fish fed on the β-CG diets upregulated significantly the expression of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and eIF4E-binding protein (4E-BP) in the proximal intestine (PI) than those fed on the CON diet (P < 0.05). The fish fed on the β-CG2 diet decreased significantly the expression of transforming growth factor beta 1 (TGFβ1) in the PI compared to those fed on the CON diet. The fish fed on the β-CG diets downregulated significantly the expression of target of rapamycin (TOR) in the PI than those fed on the CON diet. The fish fed on β-CG diets downregulated significantly the expression of AMP-activated protein kinase alpha (AMPK), acetyl-CoA carboxylase (ACC), TOR in the mid intestine (MI) while, claudin11 gene was significantly increased (P < 0.05). In the distal intestine (DI), feeding the fish on the β-CG diets downregulated significantly the expression of AMPK and ACC genes, while increased the expression TNF-α, IL-1β and claudin11 (P < 0.05). Feeding the fish with the β-CG diets mostly altered glycerophospholipid metabolism and arginine biosynthesis in intestinal mucosa. These results suggest that dietary β-CG induces enteritis in different intestinal segments and changes glycerophospholipid metabolism and arginine biosynthesis pathways. Fish farmers using soybean meal in the diets should process the ingredients to reduce β-CG concentration before use.

Antihypertensive Effect of Dietary β-Conglycinin in the Spontaneously Hypertensive Rat (SHR).

Dietary β-conglycinin has been shown to increase plasma adiponectin concentration and decrease visceral adipose tissue weight in rats. Since adiponectin is one of the factors regulating blood pressure, as well as modulating lipid metabolism, we examined whether dietary β-conglycinin affects blood pressure in spontaneously hypertensive rats. The experimental diets were prepared according to the AIN-93G formula containing 20% protein, either casein (Control) or casein replaced with soy protein isolate (SOY) or β-conglycinin (β-CON) at the proportion of 50%. Male rats (SHR/Izm, 6 wk-old) were fed the diets for 7 weeks. The SOY compared with the Control significantly suppressed the blood pressure both at week 4 (p = 0.011, Control vs. SOY) and thereafter, and β-CON had even higher suppression (p = 0.0002, Control vs. β-CON). SOY and β-CON increased plasma adiponectin concentration followed by an increase in plasma nitric oxide and possibly a decreasing trend of gene expressions of angiotensinogen in the liver and renin in the kidney. The results indicated suppression by β-conglycinin of increasing blood pressure through an enhancement of plasma adiponectin, probably in combination with a regulation of the renin–angiotensin system in spontaneously hypertensive rats.

Effects of β‐Conglycinin on intestinal structure and intestinal permeability in Rhynchocypris lagowski Dybowski

The purpose of this study was to evaluate the effects of β-conglycinin on intestinal permeability, intestinal morphology and the expression of tight junction protein in Rhynchocypris lagowski Dybowski. 750 Rhynchocypris lagowski Dybowski (4.61 ± 0.01 g) were divided into 5 groups (CK, β-20, β-40, β-60 and β-80 groups) and fed with 5 diets contained, respectively (0, 20, 40, 60 and 80 g/kg), β-conglycinin for 8 weeks. These results showed dietary β-conglycinin could destroy the structural integrity of intestine, cause villus to break and shrink, and the epithelium and lamina propria to separate. Simultaneously, compared with CK group, the levels of Diamine oxidase (DAO), 5-Hydroxytryptamine (5-HT), D-lactic acid (D-LA) and Endothelin-1 (ET-1) in serum were significantly increased in β-20, β-40, β-60 and β-80 groups (P < .05). In proximal intestines (PI), the expression of Zonula occludens-1 (ZO-1) and Occludin-b was significantly reduced, and lamina propria width was significantly increased in β-60 and β-80 groups (P < .05), and fold height, muscular layer thickness and the expression of Claudin were significantly decreased in β-40, β-60 and β-80 groups (P < .05), and the expression of Occludin-a was significantly decreased in β-20, β-40, β-60 and β-80 groups (P < .05); in addition, the expression of ZO-1 in PI was significantly increased in β-20 and β-40 groups (P < .05). In mid intestines (MI), fold height and the expression of ZO-1 and Claudin were significantly reduced, and lamina propria width was significantly increased in β-40, β-60 and β-80 groups (P < .05), and the expression of ZO-1 was significantly increased in β-20 groups (P < .05), and muscular layer thickness and the expression of Occludin-a and Occludin-b were significantly decreased in β-20, β-40, β-60 and β-80 groups (P < .05). In distal intestines (DI), fold height and the expression of ZO-1, Claudin, Occludin-a and Occludin-b were significantly reduced, and lamina propria width was significantly increased in β-20, β-40, β-60 and β-80 groups (P < .05), and muscular layer thickness was significantly reduced in β-40, β-60 and β-80 groups (P < .05). In summary, dietary β-conglycinin had negative effects on tight junctions, intestinal permeability and morphology. Moreover, the negative effects of β-conglycinin on intestines from high to low were DI, MI and PI in our study.

Dynamics of Intestinal Inflammatory Cytokines and Tight Junction Proteins of Turbot (Scophthalmus maximus L.) During the Development and Recovery of Enteritis Induced by Dietary β-Conglycinin

This study was conducted to investigate the dynamics characterization of enteritis of juvenile turbot (Scophthalmus maximus L.), during the development of enteritis induced by dietary β-conglycinin and the recovery by fish meal. Two isonitrogenous and isolipidic experimental diets were formulated, fish meal (FM) diet and fish meal supplemented with 8% β-conglycinin (7S) diet. The feeding trial consist of three groups, (1) turbot fed FM and 7S diet for ten weeks respectively, (2) turbot fed 7S diet for three weeks and then fed FM diet for another seven weeks (7S&FM). The distal intestines and serum of turbot in 7S&FM group were sampled at the 0 day, 3rd day, 1st week, 2nd week, 3rd week, 6th week and 10th week. After ten weeks feeding, the growth performance and feed utilization of turbot in FM and 7S&FM group were significantly higher than that of turbot in 7S group. According to the observation of intestine histology, the typical symptoms of enteritis were observed in the third week and then mitigated by fish meal gradually until the tenth week. The activities of DAO and content of D-lactate in serum showed the similar trend in ten weeks. The gene expression of pro-inflammatory cytokines IL-1β, IL-8, IL-22 and IFN-γ was significantly increased by 7S in the first three weeks and then significantly decreased by FM since the sixth week, as well as the expression of NF-κB. The opposite trend of gene expression was observed in anti-inflammatory cytokine TGF-β. The gene expression of tight junction proteins claudin-3, claudin-4, claudin-like, occludin and ZO-1 was significantly decreased during the first three weeks and then the gene expression of claudin-4 and occludin was significantly increased by dietary fish meal since the sixth week. Meanwhile, the gene expression of MLCK increased significantly during the first three weeks and then significantly declined at the tenth week. Collectively, dietary 8% β-conglycinin could induce the serious enteritis of turbot in three weeks and the mitigation progress could be observed when turbot fed fish meal diet. The intestinal inflammatory cytokines and tight junction proteins showed different responses during the development and recovery of enteritis.

The dynamic process of dietary soybean β-conglycinin in digestion, absorption, and metabolism among different intestinal segments in grass carp (Ctenopharyngodon idella).

The present study aimed to investigate the dynamic process of soybean β-conglycinin in digestion, absorption, and metabolism in the intestine of grass carp (Ctenopharyngodon idella). Fish fed with 80g β-conglycinin/kg diet for 7weeks, the intestinal digestive enzyme was extracted to hydrolyze β-conglycinin in vitro, the free amino acid and its metabolism product contents in intestinal segments were analyzed. The present study first found that β-conglycinin cannot be thoroughly digested by fish intestinedigestive enzyme and produces new products (about 60- and 55-kDa polypeptides). The indigestible β-conglycinin further caused the free amino acid imbalance, especially caused free essential amino acid deficiency in the proximal intestine but excess in the distal intestine. Moreover, these results might be partly associated with the effect of β-conglycinin in amino acid transporters and tight junction-regulated paracellular pathway. Finally, dietary β-conglycinin increased the content of amino acid catabolism by-product ammonia while decreased the amino acid anabolism product carnosine content in the proximal intestine and distal intestine. Thus, the current study first and systemically explored the dynamic process of β-conglycinin in digestion, absorption, and metabolism, which further supported our previous study that dietary β-conglycinin suppressed fish growth and caused intestine injure.

Soybean β-conglycinin caused intestinal inflammation and oxidative damage in association with NF-κB, TOR and Nrf2 in juvenile grass carp (Ctenopharyngodon idella): varying among different intestinal segments

The current study aimed to investigate the effects and mechanisms of dietary soybean β-conglycinin in immune function and oxidative damage among different intestinal segments of juvenile grass carp (Ctenopharyngodon idella). 240 fish (13.77 ± 0.10 g) were fed control or 8% β‐conglycinin diet for 7 weeks. Dietary β-conglycinin caused inconsistent suppression effects on the innate immune by decreasing complement component, lysozyme, antimicrobial peptide and acid phosphatase among different intestinal segments. Meanwhile, dietary β-conglycinin caused inflammation in the mid and distal intestine by raising pro-inflammatory cytokines and declining anti-inflammatory cytokines mRNA levels, while more serious in the distal intestine than in the mid intestine. Furthermore, dietary β-conglycinin regulating inflammatory cytokines might be associated with transcription factors nuclear factor-κB P65 (NF-κB P65) nucleus translocation and target of rapamycin (TOR) phosphorylation in the distal intestine but only related to TOR phosphorylation in the mid intestine. Interestingly, in the proximal intestine, dietary β-conglycinin decreased both pro-inflammatory and anti-inflammatory cytokines mRNA level, and did not affect NF-κB P65 nucleus translocation and TOR phosphorylation. For oxidative damage, dietary β-conglycinin exposure elevated both malondialdehyde (MDA) and protein carbonyl (PC) contents in the distal intestine, which might be attributed to the suppression of the Mn-SOD, catalase (CAT) and glutathione peroxidase (GPx) activities. In the mid intestine, dietary β-conglycinin only increased PC content in association with the low activities of CAT, GPx and glutathione peroxidase (GR). Unexpectedly, in the proximal intestine, dietary β-conglycinin did not significantly change MDA and PC contents while decreased antioxidant enzyme activities. Furtherly, dietary β-conglycinin affect the antioxidant enzyme activity might be regulated by the varying pattern of nuclear factor-erythroid 2-related factor 2 (Nrf2) nucleus translocation among these three intestinal segments. In summary, dietary β-conglycinin caused intestinal inflammation and oxidative damage in association with NF-κB, TOR and Nrf2 signaling molecules, which were varying among the three intestinal segments of grass carp.

Improvement of dietary N-acetylcysteine on growth inhibition and intestinal damage induced by β-conglycinin in juvenile Chinese mitten crabs (Eriocheir sinensis)

β-conglycinin is a major component of feed allergens that can cause inflammation and dysfunction of intestinal digestion and absorption in fish, but little is known in crab. This study investigated the mitigative effects of N-acetylcysteine (NAC) on growth inhibition and intestinal damage induced by β-conglycinin in juvenile Chinese mitten crabs (Eriocheir sinensis). All three experimental diets contained 70 g/kg β-conglycinin, but with three levels of NAC in each diet (0, 0.5 and 1 g/kg respectively). The control diet did not contain β-conglycinin nor NAC, but all four diets were isonitrogenous and isolipidic. Juvenile crab (3.06 ± 0.03 g) were respectively fed with these diets for eight weeks. Dietary inclusion of 1 g/kg NAC significantly improved crab survival and weight gain than those of the negative control, and showed no difference with the control group. The crabs fed diets containing β-conglycinin had lower glutathione and catalase activities but higher malondialdehyde in the intestine than those in the control group. Moreover, dietary β-conglycinin improved the level of histamine in the intestine and increased the activity of diamine oxidase in serum. The activities of lipase in hepatopancreas and trypsin in both hepatopancreas and intestine were restrained by β-conglycinin, while addition of NAC reversed these negative effects. The addition of NAC restored the impaired immunity and morphological structure of the intestine. Moreover, dietary NAC downregulated mRNA levels of pro-inflammatory factor genes (lipopolysaccharide-induced TNF-α factor, EsRelish and interleukin-2 enhancer-binding factor 2) while upregulated the structural integrity peritrophic membrane related gene expression levels (peritrophin-like gene, peritrophic 1 and 2). This study indicates that N-acetylcysteine is a useful feed additive to ameliorate the growth inhibition, intestinal oxidative damage and inflammation induced by β-conglycinin in crab diets.

Effects of β‐conglycinin on growth performance, antioxidant capacity and intestinal health in juvenile golden crucian carp,Carassius auratus

The objective of this study was conducted to research the effects of β-conglycinin in the diets on the growth performance, immunity function, antioxidant capacity and intestinal health of juvenile golden crucian carp (Carassius auratus). Five diets contained respectively (0, 20, 40, 60 and 80 g/kg) β-conglycinin, and were used to feed juvenile golden crucian carp for 56 days. Final weight, weight gain and specific growth rate were significantly reduced by dietary β-conglycinin (20–80 g/kg). Feed efficiency and protein efficiency were significantly reduced by dietary β-conglycinin (40–80 g/kg). In hepatopancreas, the activities of T-SOD, ACP, ALT and T-AOC were significantly suppressed by dietary β-conglycinin (20–80 g/kg). The activities of LZM, AKP, CAT and GPx were significantly reduced by dietary β-conglycinin (40–80 g/kg). The activities of protease were significantly reduced and the content of MDA was significantly increased by dietary β-conglycinin (60–80 g/kg). In proximal intestines, the activities of protease and CAT were significantly decreased by dietary β-conglycinin (40–80 g/kg). In mid and distal intestines, the activities of protease and CAT were significantly inhibited by dietary β-conglycinin (20–80 g/kg). In intestines, T-AOC and GPx were significantly declined by dietary β-conglycinin (20–80 g/kg). In proximal and mid intestines, the content of MDA were significantly increased by dietary β-conglycinin (40–80 g/kg). In distal intestines, the content of MDA was significantly increased by dietary β-conglycinin (20–80 g/kg). The expression of IGF-I was significantly decreased and the expression of IL-1β and TNF-α was significantly increased by dietary β-conglycinin (20–80 g/kg). The structural integrity of intestinal tissues were damaged by dietary β-conglycinin (20–80 g/kg), the part of intestinal villus were shed, the part of epithelial cells were separated from lamina propria. Ultimately, these results suggested dietary β-conglycinin should be <20 g/kg in formula feed of golden crucian carp.

Dietary β-Conglycinin Modulates Insulin Sensitivity, Body Fat Mass, and Lipid Metabolism in Obese Otsuka Long-Evans Tokushima Fatty (OLETF) Rats.

The physiological effects of dietary β-conglycinin (β-CON), one of the major components of soy protein (SOY), were examined in an obese animal model. Prior studies show that β-CON intake decreases plasma triglycerides and visceral adipose tissue weight, and increases plasma adiponectin in rodents. Since plasma adiponectin is known to affect both lipid and glucose metabolism, feeding a diet containing β-CON could modulate insulin sensitivity. Therefore, we examined the effects of dietary β-CON on insulin sensitivity and blood glucose levels, as well as lipid metabolism in obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats (pre-symptomatic stage of type 2 diabetes mellitus). Male OLETF rats (6 weeks old) were fed diets containing 20% protein such as casein (CAS), CAS replaced with soy protein (SOY), or β-CON at a proportion of 50% for 13 weeks. Fasting blood glucose levels were measured every 3 weeks, and an insulin tolerance test (ITT; 0.75 IU/kg body weight) was conducted at week 12. During the feeding period, fasting blood glucose was comparable among the groups. Insulin sensitivity measured by the ITT revealed that the SOY and β-CON diets decreased blood glucose levels at 30 min after intraperitoneal insulin injection (vs. CAS diet). In addition, the β-CON diet increased plasma adiponectin concentrations, hepatic gene expression of insulin receptor substrate (IRS) 2, and muscle gene expression of adiponectin receptor 1 (AdipoR1) and IRS1, and with a decrease in plasma insulin concentration. Finally, the β-CON diet decreased the mesenteric adipose tissue weight and liver triglyceride concentration compared to the CAS diet. These results suggest that the metabolic effects of dietary β-CON are mediated by increasing plasma adiponectin to increase insulin sensitivity and influence the hepatic lipid metabolism in obese OLETF rats.

Effects of glycinin and β-conglycinin on growth performance and intestinal health in juvenile Chinese mitten crabs (Eriocheir sinensis)

This study investigates the effects of two soybean antigens (glycinin and β-conglycinin) as an antinutritional substance in the diet on the growth, digestive ability, intestinal health and microbiota of juvenile Chinese mitten crabs (Eriocheir sinensis). The isonitrogenous and isolipidic diets contained two soybean antigens at two levels each (70 and 140 g/kg β-conglycinin, 80 and 160 g/kg glycinin) and a control diet without β-conglycinin or glycinin supplementation, and were used respectively to feed juvenile E. sinensis for seven weeks. Dietary inclusion of either glycinin or β-conglycinin significantly reduced crab survival and weight gain. The crabs fed diets containing soybean antigens had higher malondialdehyde concentrations and lower catalase activities in the intestine than those in the control. The activities of trypsin and amylase in the intestine were suppressed by dietary β-conglycinin and glycinin. Dietary glycinin or β-conglycinin impaired the immunity and morphological structure of intestine, especially the peritrophic membrane. The mRNA expression of constitutive and inducible immune responsive genes (lipopolysaccharide-induced TNF-α factor and interleukin-2 enhancer-binding factor 2) increased while the mRNA expression of the main genes related to the structural integrity peritrophic membrane (peritrophin-like gene and peritrophic 2) significantly decreased in the groups with soybean antigen addition. Soybean antigen could also change the intestinal microbial community. The abundance of pathogenic bacteria (Ochrobactrum, Burkholderia and Pseudomonas) increased significantly in both soybean antigen groups. Although pathogenic bacteria Vibrio were up-regulated in the glycinin group, the abundance of Dysgonomonas that degraded lignocellulose and ameliorated the gut environment decreased in the glycinin group. This study indicates that existence of soybean antigens (glycinin or β-conglycinin) could induce gut inflammation, reshape the community of gut microbiota, and cause digestive dysfunction, ultimately leading to impaired growth in crabs.

Dietary β-conglycinin prevents acute ethanol-induced fatty liver in mice

Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. β-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether β-conglycinin feeding has an effect on the prevention of acute ethanol-induced fatty liver in mice. Male C57BL/6J mice were fed with 20 energy% β-conglycinin or casein for 4 weeks prior to ethanol administration and were then given ethanol or glucose, as a control, by gavage. Ethanol significantly increased liver triglyceride (TG) in mice fed casein due to the activation of peroxisome proliferator-activated receptor (PPAR) γ2, a nuclear transcription factor known for regulating lipid metabolism and de novo lipogenesis. The liver TG of ethanol-administered β-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed β-conglycinin. The increased levels of PPARγ2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed β-conglycinin. Moreover, β-conglycinin decreased the basal expression of de novo lipogenesis-related genes such as stearoyl-CoA desaturase-1, and therefore, the expressions of these genes were lower in the ethanol-administered β-conglycinin-fed mice than in the casein-fed mice. In conclusion, β-conglycinin supplementation appears to prevent the development of fatty liver in mice caused by ethanol consumption via the suppression of alcohol-induced activation of PPARγ2 and the downregulation of the basal expression of de novo lipogenesis.

Dietary soya allergen β-conglycinin induces intestinal inflammatory reactions, serum-specific antibody response and growth reduction in a carnivorous fish species, turbot Scophthalmus maximus L.

This study was conducted to investigate the effects of dietary β-conglycinin on the growth performance, digestion, gut morphology and immune responses of juvenile turbot (Scophthalmus maximus L.). Four diets were formulated to contain 0%, 2%, 4% and 8% purified β-conglycinin. Triplicate groups of 30 fish were fed to apparent satiation twice daily for 12 weeks. Fish fed 4% and 8% dietary β-conglycinin showed significantly reduced specific growth rate, feed efficiency ratio, apparent digestibility coefficient of nutrients and whole-body lipid contents, as well as a profound infiltration of mixed leucocytes in the lamina propria and a significant decrease in the absorptive surface of distal intestine. The expression of pro-inflammatory cytokines, TNF-α and IL-1β, in the distal intestine was significantly upregulated by 4% dietary β-conglycinin, whereas a significantly lower expression level of IgM and anti-inflammatory cytokine TGF-β1 was observed in fish fed 8% dietary β-conglycinin. Serum lysozyme and alternative complement pathway activity were first significantly enhanced by 2% dietary β-conglycinin and then rapidly declined by 4% and 8% dietary β-conglycinin. Respiratory burst activity of head kidney macrophages and serum superoxide dismutase activity were significantly suppressed by 4% and 8% dietary β-conglycinin. Dietary β-conglycinin (2–8%) significantly increased the level of specific antibody against β-conglycinin in serum. Collectively, these results suggested that higher levels of dietary β-conglycinin (4–8%) induced a variety of non-specific and specific immune responses and intestinal mucosal lesions in turbot, resulting in inferior feed utilization and poor growth performance.

Single ingestion of soy β-conglycinin induces increased postprandial circulating FGF21 levels exerting beneficial health effects.

Soy protein β-conglycinin has serum lipid-lowering and anti-obesity effects. We showed that single ingestion of β-conglycinin after fasting alters gene expression in mouse liver. A sharp increase in fibroblast growth factor 21 (FGF21) gene expression, which is depressed by normal feeding, resulted in increased postprandial circulating FGF21 levels along with a significant decrease in adipose tissue weights. Most increases in gene expressions, including FGF21, were targets for the activating transcription factor 4 (ATF4), but not for peroxisome proliferator-activated receptor α. Overexpression of a dominant-negative form of ATF4 significantly reduced β-conglycinin-induced increases in hepatic FGF21 gene expression. In FGF21-deficient mice, β-conglycinin effects were partially abolished. Methionine supplementation to the diet or primary hepatocyte culture medium demonstrated its importance for activating liver or hepatocyte ATF4-FGF21 signaling. Thus, dietary β-conglycinin intake can impact hepatic and systemic metabolism by increasing the postprandial circulating FGF21 levels.

Effects of dietary β-conglycinin and glycinin on digestive enzymes activities, intestinal histology and immune responses of juvenile turbotScophthalmus maximus

Effects of dietary β-conglycinin and glycinin on digestive enzymes activities, intestinal histology and immune responses of juvenile turbot<i>Scophthalmus maximus</i>

Dietary β-conglycinin prevents fatty liver induced by a high-fat diet by a decrease in peroxisome proliferator-activated receptor γ2 protein

Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). Mice fed a high-fat diet, especially that of saturated-fat-rich oil, develop fatty liver with an increase in peroxisome proliferator-activated receptor (PPAR) γ2 protein in liver. The fatty liver induced by a high-fat diet is improved by knockdown of liver PPARγ2. In this study, we investigated whether β-conglycinin (a major protein of soy protein) could reduce PPARγ2 protein and prevent high-fat-diet-induced fatty liver in ddY mice. Mice were fed a high-starch diet (70 energy% [en%] starch) plus 20% (wt/wt) sucrose in their drinking water or a high-safflower-oil diet (60 en%) or a high-butter diet (60 en%) for 11 weeks, by which fatty liver is developed. As a control, mice were fed a high-starch diet with drinking water. Either β-conglycinin or casein (control) was given as dietary protein. β-Conglycinin supplementation completely prevented fatty liver induced by each type of diet, along with a reduction in adipose tissue weight. β-Conglycinin decreased sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP) messenger RNAs (mRNAs) in sucrose-supplemented mice, whereas it decreased PPARγ2 mRNA (and its target genes CD36 and FSP27), but did not decrease SREBP-1c and ChREBP mRNAs, in mice fed a high-fat diet. β-Conglycinin decreased PPARγ2 protein and liver triglyceride (TG) concentration in a dose-dependent manner in mice fed a high-butter diet; a significant decrease in liver TG concentration was observed at a concentration of 15 en%. In conclusion, β-conglycinin effectively prevents fatty liver induced by a high-fat diet through a decrease in liver PPARγ2 protein.

Characterization of the antigenic specificity of soybean protein β-conglycinin and its effects on growth and immune function in rats

The objective of the present study was to characterize the antigenic specificity of purified soybean β-conglycinin and to investigate its effects on the growth and immune responses of rats. Thirty-two Brown Norway rats, 3 weeks of age, were randomly allotted to one of four treatments and individually fed casein-cornstarch based diets. Rats were sensitised by means of intragastric gavage with purified β-conglycinin (0, 5, 10 or 20 mg protein/ml in phosphate buffered saline at pH 7.4) on day 0, 7, 14, and 21 (1 ml/animal). On day 28, rats received a double dose of β-conglycinin. Blood was obtained at weekly intervals after initiation of challenge. Growth declined linearly with increasing the concentration of soybean β-conglycinin (p < 0.05). Both the total IgE and β-conglycinin-specific IgE levels in serum increased while passive cutaneous anaphylactic reactions were induced in the rats. Lymphocyte proliferation response to concanavalin A in plasma and spleen was increased linearly with increased levels of soybean (p < 0.01) β-conglycinin. The percentage of CD4+ lymphocyte subset linearly increased (p < 0.001). As a result, the concentrations of cytokines in plasma and spleen, including interleukin-4 (p < 0.01), interleukin-5 (p < 0.01), and tumour necrosis factor-α (p < 0.01) increased linearly with increasing level of purified β-conglycinin. Our results indicate that purified β-conglycinin possesses intrinsic immune-stimulating capacity and can induce an allergic reaction. Therefore, dietary soybean β-conglycinin has negative effects on growth and both cell-mediated and humoral immune function in rats.