Changes In Intestinal Metabolism Research Articles

Significant alterations of intestinal symbiotic microbiota induced by intraperitoneal vaccination mediate changes in intestinal metabolism of NEW Genetically Improved Farmed Tilapia (NEW GIFT, Oreochromis niloticus)

BackgroundAfter millions of years of coevolution, symbiotic microbiota has become an integral part of the host and plays an important role in host immunity, metabolism, and health. Vaccination, as an effective means of preventing infectious diseases, has been playing a vital role in the prevention and control of human and animal diseases for decades. However, so far, minimal is known about the effect of vaccination on fish symbiotic microbiota, especially mucosal microbiota, and its correlation with intestinal metabolism remains unclear.MethodsHere we reported the effect of an inactivated bivalent Aeromonas hydrophila/Aeromonas veronii vaccine on the symbiotic microbiota and its correlation with the intestinal metabolism of farmed adult Nile tilapia (Oreochromis niloticus) by 16S rRNA gene high-throughput sequencing and gas chromatography-mass spectrometry metabolomics.ResultsResults showed that vaccination significantly changed the structure, composition, and predictive function of intestinal mucosal microbiota but did not significantly affect the symbiotic microbiota of other sites including gill mucosae, stomach contents, and stomach mucosae. Moreover, vaccination significantly reduced the relative abundance values of potential opportunistic pathogens such as Aeromonas, Escherichia–Shigella, and Acinetobacter in intestinal mucosae. Combined with the enhancement of immune function after vaccination, inactivated bivalent Aeromonas vaccination had a protective effect against the intestinal pathogen infection of tilapia. In addition, the metabolite differential analysis showed that vaccination significantly increased the concentrations of carbohydrate-related metabolites such as lactic acid, succinic acid, and gluconic acid but significantly decreased the concentrations of multiple lipid-related metabolites in tilapia intestines. Vaccination affected the intestinal metabolism of tilapia, which was further verified by the predictive function of intestinal microbiota. Furthermore, the correlation analyses showed that most of the intestinal differential microorganisms were significantly correlated with intestinal differential metabolites after vaccination, confirming that the effect of vaccination on intestinal metabolism was closely related to the intestinal microbiota.ConclusionsIn conclusion, this paper revealed the microbial and metabolic responses induced by inactivated vaccination, suggesting that intestinal microbiota might mediate the effect of vaccination on the intestinal metabolism of tilapia. It expanded the novel understanding of vaccine protective mechanisms from microbial and metabolic perspectives, providing important implications for the potential influence of vaccination on human intestinal microbiota and metabolism.-tufGxbkxhm-UiFTxxYHNiVideo

Effects of Aroclor 1254 on Intestinal Immunity, Metabolism, and Microflora in Zebrafish.

Polychlorinated biphenyls (PCBs) are widely distributed environmental toxicants, whose biological toxicity is magnified step by step through the transmission of the food chain. However, there is little research about the effect of PCBs on intestinal epithelial barrier function. In this experiment, the effects of PCB exposure on the intestines of zebrafish were evaluated. Animals were exposed to Aroclor 1254 (5 μg/L, 10 μg/L, 15 μg/L). After 21 days, the changes in histology, enzyme biomarkers, intestinal microorganisms, and metabolomics were detected. The inflammation and oxidative stress in the intestines of zebrafish were observed. Additionally, there were significant changes in intestinal microbiota and tissue metabolism, most of which were associated with oxidative stress, inflammation, and lipid metabolism. The results showed that PCBs exposure resulted in intestinal inflammation and oxidative stress in zebrafish.Moreover, intestinal metabolites and intestinal microflora of zebrafish were also disturbed. This study verified that exposure can lead to intestinal damage and changes in intestinal metabolic capacity and microorganisms, enlightening the consequences of PCB exposure.

Omega-3 Phospholipids from Krill Oil Enhance Intestinal Fatty Acid Oxidation More Effectively than Omega-3 Triacylglycerols in High-Fat Diet-Fed Obese Mice.

Antisteatotic effects of omega-3 fatty acids (Omega-3) in obese rodents seem to vary depending on the lipid form of their administration. Whether these effects could reflect changes in intestinal metabolism is unknown. Here, we compare Omega-3-containing phospholipids (krill oil; ω3PL-H) and triacylglycerols (ω3TG) in terms of their effects on morphology, gene expression and fatty acid (FA) oxidation in the small intestine. Male C57BL/6N mice were fed for 8 weeks with a high-fat diet (HFD) alone or supplemented with 30 mg/g diet of ω3TG or ω3PL-H. Omega-3 index, reflecting the bioavailability of Omega-3, reached 12.5% and 7.5% in the ω3PL-H and ω3TG groups, respectively. Compared to HFD mice, ω3PL-H but not ω3TG animals had lower body weight gain (−40%), mesenteric adipose tissue (−43%), and hepatic lipid content (−64%). The highest number and expression level of regulated intestinal genes was observed in ω3PL-H mice. The expression of FA ω-oxidation genes was enhanced in both Omega-3-supplemented groups, but gene expression within the FA β-oxidation pathway and functional palmitate oxidation in the proximal ileum was significantly increased only in ω3PL-H mice. In conclusion, enhanced intestinal FA oxidation could contribute to the strong antisteatotic effects of Omega-3 when administered as phospholipids to dietary obese mice.

Exercise Training Modulates Gut Microbiota Profile and Improves Endotoxemia.

Intestinal metabolism and microbiota profiles are impaired in obesity and insulin resistance. Moreover, dysbiotic gut microbiota has been suggested to promote systemic low-grade inflammation and insulin resistance through the release of endotoxins particularly lipopolysaccharides. We have previously shown that exercise training improves intestinal metabolism in healthy men. To understand whether changes in intestinal metabolism interact with gut microbiota and its release of inflammatory markers, we studied the effects of sprint interval (SIT) and moderate-intensity continuous training (MICT) on intestinal metabolism and microbiota in subjects with insulin resistance. Twenty-six, sedentary subjects (prediabetic, n = 9; type 2 diabetes, n = 17; age, 49 [SD, 4] yr; body mass index, 30.5 [SD, 3]) were randomized into SIT or MICT. Intestinal insulin-stimulated glucose uptake (GU) and fatty acid uptake (FAU) from circulation were measured using positron emission tomography. Gut microbiota composition was analyzed by 16S rRNA gene sequencing and serum inflammatory markers with multiplex assays and enzyme-linked immunoassay kit. V˙O2peak improved only after SIT (P = 0.01). Both training modes reduced systematic and intestinal inflammatory markers (tumor necrosis factor-α, lipopolysaccharide binding protein) (time P < 0.05). Training modified microbiota profile by increasing Bacteroidetes phylum (time P = 0.03) and decreasing Firmicutes/Bacteroidetes ratio (time P = 0.04). Moreover, there was a decrease in Clostridium genus (time P = 0.04) and Blautia (time P = 0.051). Only MICT decreased jejunal FAU (P = 0.02). Training had no significant effect on intestinal GU. Colonic GU associated positively with Bacteroidetes and inversely with Firmicutes phylum, ratio Firmicutes/Bacteroidetes and Blautia genus. Intestinal substrate uptake associates with gut microbiota composition and whole-body insulin sensitivity. Exercise training improves gut microbiota profiles and reduces endotoxemia.

Role of gut peptide in diabetes remission after Roux-en-Y gastric bypass surgery

Roux-en-Y gastric bypass surgery results in the resolution of type 2 diabetes in ∼60% of cases. Pre-surgery beta-cell function, with the large and sustained weight loss resulting from the surgery, are the main predictors of diabetes remission. However, enteric mechanisms, independent of weight loss, have been identified as important players. They include, among others, changes in intestinal metabolism, the gut hormones, the bile acids and the microbiome. The enhanced release of glucagon-like peptide 1 (GLP-1) contribute to the improvement of the incretin effect on insulin secretion during meals. GLP-1 and other gut peptides such as peptide YY and oxyntomodulin, may also contribute to the increased satiety and the decreased reward power of food observed after bypass, both contributing to decreased food intake and sustained weight loss. Although enteric factors are key for the full recovery of beta cell function during meals, the recovery of beta cell function in response to an IV glucose stimulus is more modest in magnitude, even in individual in diabetes remission. This may explain, in part, the long-term diabetes relapse in some patients. With the improvement of gut-mediated improved insulin secretion, RYGB results in large increase in insulin sensitivity and clearance, both contributors to improved glucose metabolism.

The Effects of Continuous and Intermittent Reduced Speed Modes on Renal and Intestinal Perfusion in an Ovine Model

The effects of the continuous-flow output on renal and intestinal microcirculation have not been extensively studied. To address this, the Heartware HVAD pump loaded with continuous and intermittent reduced speed (IRS) modes was implanted in four sheep and then operated at low and high speeds to mimic partial and complete unloading of the left ventricle. Then microsphere and positron emission tomography/computed tomography (PET/CT) studies were used to assess renal and intestinal tissue perfusion at various pump speeds and flow modes as compared with baseline (pump off). Arterial and venous oxygen (T02) and carbon dioxide (TCO2) contents were measured to assess changes in intestinal metabolism. Renal and intestinal regional blood flows did not produce any significant changes compared with baseline values in either continuous or IRS modes and speeds. The venous TO2 and TCO2 significantly increased in continuous and IRS modes and speeds compared with baseline. Our data suggested that renal and intestinal tissue perfusions were not adversely affected by continuous and IRS modes either in partial or complete unloading. Intestinal venous hyperoxia and increased TCO2 may be the evidence of intestinal arteriovenous shunting along with increased intestinal tissue metabolism. Longer-term studies are warranted in chronic heart failure models.

Rimonabant-mediated changes in intestinal lipid metabolism and improved renal vascular dysfunction in the JCR:LA-cprat model of prediabetic metabolic syndrome

Rimonabant (SR141716) is a specific antagonist of the cannabinoid-1 receptor. Activation of the receptor initiates multiple effects on central nervous system function, metabolism, and body weight. The hypothesis that rimonabant has protective effects against vascular disease associated with the metabolic syndrome was tested using JCR:LA-cp rats. JCR:LA-cp rats are obese if they are cp/cp, insulin resistant, and exhibit associated micro- and macrovascular disease with end-stage myocardial and renal disease. Treatment of obese rats with rimonabant (10 mg.kg(-1).day(-1), 12-24 wk of age) caused transient reduction in food intake for 2 wk, without reduction in body weight. However, by 4 wk, there was a modest, sustained reduction in weight gain. Glycemic control improved marginally compared with controls, but at the expense of increased insulin concentration. In contrast, rimonabant normalized fasting plasma triglyceride and reduced plasma plasminogen activator inhibitor-1 and acute phase protein haptoglobin in cp/cp rats. Furthermore, these changes were accompanied by reduced postprandial intestinal lymphatic secretion of apolipoprotein B48, cholesterol, and haptoglobin. While macrovascular dysfunction and ischemic myocardial lesion frequency were unaffected by rimonabant treatment, both microalbuminuria and glomerular sclerosis were substantially reduced. In summary, rimonabant has a modest effect on body weight in freely eating obese rats and markedly reduces plasma triglyceride levels and microvascular disease, in part due to changes in intestinal metabolism, including lymphatic secretion of apolipoprotein B48 and haptoglobin. We conclude that rimonabant improves renal disease and intestinal lipid oversecretion associated with an animal model of the metabolic syndrome that appears to be independent of hyperinsulinemia or macrovascular dysfunction.

Glucagon-Like Peptide 2: A Key Link between Nutrition and Intestinal Adaptation in Neonates?

This paper reviews the evidence from recent studies in young piglets to examine the hypothesis that glucagon-like peptide 2 (GLP-2) is a physiologically relevant hormonal signal linked to the intestinal adaptation associated with enteral nutrition in neonates. Observations that support the hypothesis include, 1) the GLP-2 secretory response to enteral nutrition is functional as early as late gestation, 2) parallel changes in intestinal growth and circulating GLP-2 occur in response to the quantity and composition of enteral nutrition after birth, and 3) the acute temporal changes in intestinal metabolism and circulating GLP-2 concentrations in response to enteral nutrition are generally coincident. In contrast, however, the lack of intestinal trophic responses to both pharmacological GLP-2 concentrations in the fetus and weanling pigs, and to physiological GLP-2 concentrations in neonates raises doubts concerning the physiological relevance of GLP-2 as a enterally mediated trophic signal. A more definitive test of this hypothesis will require further studies that assess the intestinal metabolic response to enteral nutrition using experimental approaches that block GLP-2 action.

Neonatal Intestinal Metabolism

In the presence of glutamine, glucose, and 3-hydroxybutyrate, glutamine is the preferred oxidative substrate in enterocytes of suckling and weaned rats. Our studies of changes in intestinal metabolism in the developing rat clearly indicate that the oxidation of substrates that enter the citric acid cycle in the form of acetyl-CoA such as glucose, fatty acid, and lipids is low during the suckling period and increases after weaning. In contrast, glutamine that enters the citric acid cycle in the form of 2-oxoglutarate is high during the suckling period and does not change during weaning. The control of the citric acid cycle appears to be the intramitochondrial [NADH]/[NAD+] ratio, which is high during the suckling period and low in the intestine of weaned rats. These studies demonstrate how evaluating changes in metabolism during a natural perturbation such as weaning can identify control mechanisms of metabolism. Finally, the changes in substrate oxidation during weaning are not controlled by the endogenous steroid burst that occurs at 16 days of age. Substrate oxidation changes only after weaning, suggesting that a change in diet is a significant factor in intestinal substrate oxidation.

Glucagon Effect on Postischemic Recovery of Intestinal Energy Metabolism

Glucagon is a potent mesenteric vasodilator, inotrope, and stimulant of intestinal metabolism that enhances survival when given during reperfusion after intestinal ischemia. However, the mechanism of improved survival is unclear and may be due to systemic hemodynamic effects rather than intestinal metabolic changes. We examined the effects of glucagon on intestinal energy metabolism during reperfusion after intestinal ischemia. Sprague-Dawley rats were subjected to 50 min intestinal ischemia by clamping the superior mesenteric artery. All received 10 ml/kg · hr 5% glucose in normal saline for 3 hr. One group ( n = 17) received 1.6 μg/kg · min glucagon for 2 hr beginning at reperfusion. Control rats ( n = 10) received only vehicle. Jejunal biopsies preischemia, end ischemia, 10, 20, 45, 80 min, and 24 hr after reperfusion were analyzed for ATP, ADP, and AMP. ATP decreased more than 60% with ischemia and recovered substantially in all animals by 10 min postischemia. ATP recovered steadily in control rats and by 24 hr was not distinguishable from baseline. In contrast, in glucagon-treated rats, ATP decreased at 20 and 45 min during reperfusion, but recovered incompletely by 24 hr after ischemia. Energy charge (EC = ([ATP] + 1/2[ADP]) ÷ ([ATP] + [ADP] + [AMP])) decreased during ischemia but recovered immediately after reperfusion in both groups, implying that energy was available, energy metabolic enzyme systems were at least partially intact, and immediate recovery was not limited by available substrate and blood flow. However, energy charge decreased slightly during glucagon infusion, suggesting increased utilization of energy or some derangement of energy metabolism. Despite the previously demonstrated survival benefit of glucagon in this model, recovery of intestinal energy metabolism was no better with glucagon treatment. Thus, recovery of intestinal energy metabolism does not appear to be linked to animal survival after ischemia. Other investigators have shown that glucagon may worsen ischemic damage when administered before or during intestinal ischemia. This study provides evidence for intestinal metabolic stimulation by glucagon after intestinal ischemia which might be detrimental if not compensated for by beneficial systemic hemodynamic effects of glucagon.

Effects of tumour necrosis factor-? (cachectin) on glucose metabolism in the rat

Intravenous administration of a single dose (20 micrograms) of recombinant tumour necrosis factor-alpha (TNF, cachectin) to rats decreased the rate of intestinal glucose absorption. In vivo, the oxidation of [U-14C]glucose to 14CO2 was significantly increased by the cytokine. In addition, [14C]lipid accumulation from [U-14C]glucose was increased both in liver and brown adipose tissue of the TNF-injected animals. The decrease observed in intestinal glucose absorption was not associated with changes in intestinal metabolism. There was no difference in glucose metabolism by isolated enterocytes from either control or TNF-injected rats whether in the absence or presence of different concentrations of the cytokine in the incubation medium. In contrast, tumour necrosis factor altered the rate of gastric emptying as measured by the gastrointestinal distribution of 3[H]inulin following an intragastric glucose load. These results suggest that the cytokine profoundly alters glucose metabolism by increasing its whole-body oxidation rate and delaying intestinal absorption through a reduced gastric emptying.

Old and new data on diarrhetic diseases in childhood I. Etiology and pathophysiology

Etiology and Pathophysiology. The present article is a comprehensive review of recent research results in the field of acute diarrhea. The most important new idea in contrast to older views is that almost all acute diarrheas are associated with a disturbance of intestinal bacterial homeostasis: overgrowth of the small intestine with apathogenic or pathogenic organisms is followed by changes in intestinal metabolism with increase in intestinal water and electrolyte secretion. Anaerobic organisms cause by enzymatic deconugation and dydroxylation of bile acids secretion of fluid into the small intestine and inhibition of fluid absorption from the large intestine. 10-OH-fatty acids, which are formed intraluminally by enzymatic hydroxylation of long-chain unsaturated fatty acids from the diet by similar anaerobic organisms, produce profuse secretion of fluid into the small intestine. The ability of numerous strains of E. coli to produce enterotoxin, which has a qualitatively similar action to cholera toxin, is now considered to be a major cause of infantile diarrhea. The separation of two completely different pathophysiologic mechanisms of E. Coli, the enterotoxic and the enteroinvasive action which are determined by extranuclear chromosomal material, is an important result of recent research. Overgrowth of the small intestine with different bacteria is followed by loss of actiivity of lactase, and later of all disaccharidases in the intestinal mucosa.