Piperine Improves Obesity By Repairing Intestinal Barrier Function And Inhibiting Fatty Acid Absorption

Abstract BackgroundCurrently, the weight loss effects of piperine have gained considerable attention; however, the underlying mechanism needs to be comprehensively elucidated. In the present study, we aimed to investigate the relationship between the weight loss effects of piperine and intestinal function. Methods Eight-week-old Sprague Dawley male rats were provided standard diet or HFD diet for 16 weeks. After, rats from the HFD group were divided into four group, including HFD, HFD with daily gavage with 2.7mg/kg body weight of piperine (PIP-L), 13.5mg/kg body weight of piperine (PIP-M), 27mg/kg body weight of piperine (PIP-H) for another 8 weeks. The fecal fat content, serum TG, FAA levels, jejunum structure and gene expression levels related to fatty acid absorption and barrier function in intestinal were detected. Then the Caco-2 cell was cultured to explore the effects of piperine on cell proliferation, differentiation, barrier function and fatty acid absorption.ResultsIn our study, piperine repaired the tight junction damage induced by obesity by downregulating jejunal tumor necrosis factor-α and reducing lipopolysaccharide-induced damage on intestinal cell proliferation, thus enhancing intestinal barrier function, which is beneficial in reducing chronic inflammation associated with obesity. In addition, piperine inhibited intestinal fatty acid absorption in both cellular and animal models. The underlying mechanism may be related to the downregulation of fatty acid absorption-related genes, fatty acid-binding protein 2 and cluster of differentiation 36, but not fatty acid transport protein 4.Conclusion The anti-obesity effect of piperine is related to the enhancement of intestinal barrier function and inhibition of intestinal fatty acid absorption.

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Piperine Improves Obesity by Inhibiting Fatty Acid Absorption and Repairing Intestinal Barrier Function

Plant Foods for Human Nutrition ◽

10.1007/s11130-021-00919-2 ◽

2021 ◽

Author(s):

Wenli Wang ◽

Yanhua Zhang ◽

Xiong Wang ◽

Huilian Che ◽

Yali Zhang

Keyword(s):

Fatty Acid ◽

Barrier Function ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Acid Absorption ◽

Fatty Acid Absorption

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Trifostigmanoside I, an Active Compound from Sweet Potato, Restores the Activity of MUC2 and Protects the Tight Junctions through PKCα/β to Maintain Intestinal Barrier Function

International Journal of Molecular Sciences ◽

10.3390/ijms22010291 ◽

2020 ◽

Vol 22 (1) ◽

pp. 291

Author(s):

Amna Parveen ◽

Seungho Choi ◽

Ju-Hee Kang ◽

Seung Hyun Oh ◽

Sun Yeou Kim

Keyword(s):

Tight Junctions ◽

Sweet Potato ◽

Barrier Function ◽

Intestinal Barrier ◽

Human Colon ◽

Underlying Mechanism ◽

Intestinal Barrier Function ◽

Isolation And Identification ◽

Human Colon Cancer ◽

Mucin Production

Sweet potato (Ipomoea batata) is considered a superfood among vegetables and has been consumed for centuries. Traditionally, sweet potato is used to treat several illnesses, including diarrhea and stomach disorders. This study aimed to explore the protective effect of sweet potato on intestinal barrier function, and to identify the active compounds of sweet potato and their underlying mechanism of action. To this purpose, bioactivity-guided isolation, Western blotting, and immunostaining assays were applied. Interestingly, our bioactivity-guided approach enabled the first isolation and identification of trifostigmanoside I (TS I) from sweet potato. TS I induced mucin production and promoted the phosphorylation of PKCα/β in LS174T human colon cancer cells. In addition, it protected the function of tight junctions in the Caco-2 cell line. These findings suggest that TS I rescued the impaired abilities of MUC2, and protected the tight junctions through PKCα/β, to maintain intestinal barrier function.

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Sauna dehydration as a new physiological challenge model for intestinal barrier function

Scientific Reports ◽

10.1038/s41598-021-94814-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Maria Fernanda Roca Rubio ◽

Ulrika Eriksson ◽

Robert J. Brummer ◽

Julia König

Keyword(s):

Fatty Acid ◽

Intestinal Permeability ◽

Barrier Function ◽

Fatty Acid Binding Protein ◽

Binding Protein ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Fatty Acid Binding ◽

Acid Binding Protein

AbstractThe intestinal barrier plays a crucial role in maintaining gut health, and an increased permeability has been linked to several intestinal and extra-intestinal disorders. There is an increasing demand for interventions aimed at strengthening this barrier and for in vivo challenge models to assess their efficiency. This study investigated the effect of sauna-induced dehydration on intestinal barrier function (clinicaltrials.gov: NCT03620825). Twenty healthy subjects underwent three conditions in random order: (1) Sauna dehydration (loss of 3% body weight), (2) non-steroidal anti-inflammatory drug (NSAID) intake, (3) negative control. Intestinal permeability was assessed by a multi-sugar urinary recovery test, while intestinal damage, bacterial translocation and cytokines were assessed by plasma markers. The sauna dehydration protocol resulted in an increase in gastroduodenal and small intestinal permeability. Presumably, this increase occurred without substantial damage to the enterocytes as plasma intestinal fatty acid-binding protein (I-FABP) and liver fatty acid-binding protein (L-FABP) were not affected. In addition, we observed significant increases in levels of lipopolysaccharide-binding protein (LBP), IL-6 and IL-8, while sCD14, IL-10, IFN-ɣ and TNF-α were not affected. These results suggest that sauna dehydration increased intestinal permeability and could be applied as a new physiological in vivo challenge model for intestinal barrier function.

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Modulation of gut microbiota and intestinal barrier function during alleviation of antibiotic-associated diarrhea with Rhizoma Zingiber officinale (Ginger) extract

Food & Function ◽

10.1039/d0fo01536a ◽

2020 ◽

Vol 11 (12) ◽

pp. 10839-10851

Author(s):

Zhi-jie Ma ◽

Huan-jun Wang ◽

Xiao-jing Ma ◽

Yue Li ◽

Hong-jun Yang ◽

...

Keyword(s):

Gut Microbiota ◽

Barrier Function ◽

Intestinal Barrier ◽

Zingiber Officinale ◽

Underlying Mechanism ◽

Intestinal Barrier Function ◽

Ginger Extract ◽

Beneficial Effects ◽

Antibiotic Associated Diarrhea

Ginger extract showed beneficial effects on rats with antibiotic-associated diarrhea, and the underlying mechanism might be associated with the recovery of gut microbiota and intestinal barrier function.

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2’-fucosyllactose (2’-FL) Supplementation Improves Gut Barrier Function and Lipid Metabolism in HF-fed Mice

Current Developments in Nutrition ◽

10.1093/cdn/nzaa045_058 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 425-425

Author(s):

Sunhye Lee ◽

Michael Goodson ◽

Wendie Vang ◽

Karen Kalanetra ◽

Daniela Barile ◽

...

Keyword(s):

Body Weight ◽

Lipid Metabolism ◽

Intestinal Permeability ◽

Barrier Function ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Gut Barrier ◽

Low Fat ◽

Barrier Integrity ◽

Gut Barrier Function

Abstract Objectives 2’-fucosyllactose (2’-FL), the most predominant oligosaccharide found in human milk, acts as a prebiotic with beneficial effects on the host. The aim of this study was to determine the beneficial effect of 2’-FL on intestinal barrier integrity and metabolic functions in low-fat (LF)- and high-fat (HF)-fed mice. Methods Male C57/BL6 mice (n = 32, 8/group; 6 weeks old, JAX, CA) were counter-balanced into four weight-matched groups and fed either a low-fat (LF; 10% kcal fat with 7% kcal sucrose) or HF (45% kcal fat with 17% kcal sucrose) with or without supplementation of 2’-FL in the diet [10% (w/w), 8 weeks; LF/2’-FL or HF/2’-FL; BASF, Germany]. General phenotypes (body weight, energy intake, fat and lean mass), intestinal permeability (ex vivo in Ussing chambers), lipid profiles, and microbial metabolites were assessed. Results 2’-FL significantly attenuated the HF-induced increase in body fat mass with a trend to decrease body weight gain. 2’-FL significantly decreased intestinal permeability in LF-fed mice with a trend for a decrease in HF-fed mice. This was associated with a significant increase in interleukin-22, a cytokine known to have a protective role in intestinal barrier function. Visceral adipocyte size was significantly decreased by 2’-FL in both LF- and HF-fed mice. 2’-FL suppressed HF-induced upregulation of adipogenic transcription factors peroxisome proliferator-activated receptor gamma and sterol regulatory element binding protein-1c in the liver. Lastly, 2’-FL supplementation led to a significant elevation of lactic acid concentration in the cecum of HF-fed mice, which is known to be a product from beneficial microbes. Conclusions 2’-FL supplementation improved gut barrier integrity and lipid metabolism in mice with and without the metabolic challenge of HF feeding. These findings support the use of 2’-FL in the control of gut barrier function and metabolic homeostasis under normal and abnormal physiological conditions. Funding Sources BASF (Germany).

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Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00029.2015 ◽

2015 ◽

Vol 308 (10) ◽

pp. G840-G851 ◽

Cited By ~ 133

Author(s):

M. Kristina Hamilton ◽

Gaëlle Boudry ◽

Danielle G. Lemay ◽

Helen E. Raybould

Keyword(s):

Body Weight ◽

Gut Microbiota ◽

Large Intestine ◽

Barrier Function ◽

Ex Vivo ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

High Fat ◽

Ussing Chambers ◽

Diet Induced Obesity

A causal relationship between the pathophysiological changes in the gut epithelium and altered gut microbiota with the onset of obesity have been suggested but not defined. The aim of this study was to determine the temporal relationship between impaired intestinal barrier function and microbial dysbiosis in the small and large intestine in rodent high-fat (HF) diet-induced obesity. Rats were fed HF diet (45% fat) or normal chow (C, 10% fat) for 1, 3, or 6 wk; food intake, body weight, and adiposity were measured. Barrier function ex vivo using FITC-labeled dextran (4,000 Da, FD-4) and horseradish peroxidase (HRP) probes in Ussing chambers, gene expression, and gut microbial communities was assessed. After 1 wk, there was an immediate but reversible increase in paracellular permeability, decrease in IL-10 expression, and decrease in abundance of genera within the class Clostridia in the ileum. In the large intestine, HRP flux and abundance of genera within the order Bacteroidales increased with time on the HF diet and correlated with the onset of increased body weight and adiposity. The data show immediate insults in the ileum in response to ingestion of a HF diet, which were rapidly restored and preceded increased passage of large molecules across the large intestinal epithelium. This study provides an understanding of microbiota dysbiosis and gut pathophysiology in diet-induced obesity and has identified IL-10 and Oscillospira in the ileum and transcellular flux in the large intestine as potential early impairments in the gut that might lead to obesity and metabolic disorders.

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LPS Inhibits Fatty Acid Absorption in Enterocytes through TNF-α Secreted by Macrophages

Cells ◽

10.3390/cells8121626 ◽

2019 ◽

Vol 8 (12) ◽

pp. 1626 ◽

Cited By ~ 3

Author(s):

Heyuan Liu ◽

Lixia Kai ◽

Huahua Du ◽

Xinxia Wang ◽

Yizhen Wang

Keyword(s):

Fatty Acid ◽

Cell Line ◽

Conditioned Medium ◽

Caspase 3 ◽

Underlying Mechanism ◽

E Coli ◽

Acid Absorption ◽

Tnf Α ◽

Escherichia Coli Infection ◽

Fatty Acid Absorption

Diarrhea, such as steatorrhea, could result from fat absorption disorders, which could be caused by many factors, including Escherichia coli infection. However, it is not clear how E. coli affects fatty acid absorption in animals. Lipopolysaccharide (LPS), as one of the main pathogenic components of E. coli, is the main cause of the virulence of E. coli. Therefore, we used LPS to explore the underlying mechanism of E. coli that causes the inhibition of fatty acid absorption in the intestine. In this study, we found that LPS caused apoptosis of intestinal epithelial cells in mice. Further, caspase-3 activation caused the inhibition of fatty acid absorption in the intestinal porcine enterocyte cell line (IPEC-J2). However, direct treatment of LPS did not induce any significant change in fatty acid absorption in IPEC-J2. We then prepared conditioned medium of LPS-treated porcine macrophage cell line (3D4/2) for incubating IPEC-J2, as LPS initiates inflammation by activating immune cells. The conditioned medium decreased fatty acid absorption and caspase-3 activation in IPEC-J2. While inhibiting the activation of caspase-3 in IPEC-J2, conditioned medium no longer caused serious deficiency of fatty acid absorption. As IL-1β, IL-6, and TNF-α in conditioned medium increase significantly, IPEC-J2 was treated with IL-1β, IL-6, and TNF-α, respectively. Only TNF-α induced caspase-3 activation in IPEC-J2. Reducing the secretion of TNF-α in 3D4/2, there was no obvious activation of caspase-3 in IPEC-J2, and fatty acid absorption recovered effectively. Based on the above results, we hold the opinion that LPS does not suppress fatty acid absorption directly in the intestine, but may work on macrophages that secrete cytokines, such as TNF-α, inducing caspase-3 activation and finally leading to the inhibition of fatty acid absorption in intestine.

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Low Dosage of Chitosan Supplementation Improves Intestinal Permeability and Impairs Barrier Function in Mice

BioMed Research International ◽

10.1155/2016/4847296 ◽

2016 ◽

Vol 2016 ◽

pp. 1-5 ◽

Cited By ~ 3

Author(s):

Guiping Guan ◽

Hongbing Wang ◽

Hanhui Peng ◽

Guanya Li

Keyword(s):

Body Weight ◽

Feed Intake ◽

Barrier Function ◽

Control Diet ◽

Intestinal Barrier ◽

Dietary Supplementation ◽

Intestinal Barrier Function ◽

Control Group ◽

Diet Control ◽

Food And Water Intake

The purpose of this study was to explore relationships between low dose dietary supplementation with chitosan (COS) and body weight, feed intake, intestinal barrier function, and permeability in mice. Twenty mice were randomly assigned to receive an unadulterated control diet (control group) or a dietary supplementation with 30 mg/kg dose of chitosan (COS group) for two weeks. Whilst no significant differences were found between the conditions for body weight or food and water intake, mice in the COS group had an increased serum D-lactate content (P<0.05) and a decreased jejunal diamine oxidase (DAO) activity (P<0.05). Furthermore, mice in COS group displayed a reduced expression of occludin and ZO-1 (P<0.05) and a reduced expression of occludin in the ileum (P<0.05). The conclusion drawn from these findings showed that although 30 mg/kg COS-supplemented diet had no effect on body weight or feed intake in mice, this dosage may compromise intestinal barrier function and permeability. This research will contribute to the guidance on COS supplements.

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