Effects of Lactobacillus paracasei CNCM I-4034, Bifidobacterium breve CNCM I-4035 and Lactobacillus rhamnosus CNCM I-4036 on Hepatic Steatosis in Zucker Rats

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Abstract

We have previously described the safety and immunomodulatory effects of Lactobacillus paracasei CNCM I-4034, Bifidobacterium breve CNCM I-4035 and Lactobacillus rhamnosus CNCM I-4036 in healthy volunteers. The scope of this work was to evaluate the effects of these probiotic strains on the hepatic steatosis of obese rats. We used the Zucker rat as a genetic model of obesity. Zucker-Lepr ^fa/fa rats received one of three probiotic strains, a mixture of L. paracasei CNCM I-4034 and B. breve CNCM I-4035, or a placebo for 30 days. An additional group of Zucker-lean ^{+/
fa} rats received a placebo for 30 days. No alterations in intestinal histology, in the epithelial, lamina propria, muscular layers of the ileal or colonic mucosa, or the submucosae, were observed in any of the experimental groups. Triacylglycerol content decreased in the liver of Zucker-Lepr ^fa/fa rats that were fed L. rhamnosus, B. breve, or the mixture of B. breve and L. paracasei. Likewise, the area corresponding to neutral lipids was significantly smaller in the liver of all four groups of Zucker-Lepr ^fa/fa rats that received probiotics than in rats fed the placebo. Zucker-Lepr ^fa/fa rats exhibited significantly greater serum LPS levels than Zucker-lean ^{+/
fa} rats upon administration of placebo for 30 days. In contrast, all four groups of obese Zucker-Lepr ^fa/fa rats that received LAB strains exhibited serum LPS concentrations similar to those of Zucker-lean ^{+/
fa} rats. Serum TNF-α levels decreased in the Zucker-Lepr ^fa/fa rats that received B. breve, L. rhamnosus, or the mixture, whereas L. paracasei feeding decreased IL-6 levels in the serum of Zucker-Lepr ^fa/fa rats. In conclusion, the probiotic strains reduced hepatic steatosis in part by lowering serum LPS, and had an anti-inflammatory effect in obese Zucker rats.

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Banting lecture 1988. Role of insulin resistance in human disease.

G M Reaven (1988)

Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)

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Worldwide trends in childhood overweight and obesity.

Youfa Wang, Tim Lobstein (2005)

Obesity has become a global epidemic but our understanding of the problem in children is limited due to lack of comparable representative data from different countries, and varying criteria for defining obesity. This paper summarises the available information on recent trends in child overweight and obesity prevalence. PubMed was searched for data relating to trends over time, in papers published between January 1980 and October 2005. Additional studies identified by citations in retrieved papers and by consultation with experts were included. Data for trends over time were found for school-age populations in 25 countries and for pre-school populations in 42 countries. Using these reports, and data collected for the World Health Organization's Burden of Disease Program, we estimated the global prevalence of overweight and obesity among school-age children for 2006 and likely prevalence levels for 2010. The prevalence of childhood overweight has increased in almost all countries for which data are available. Exceptions are found among school-age children in Russia and to some extent Poland during the 1990s. Exceptions are also found among infant and pre-school children in some lower-income countries. Obesity and overweight has increased more dramatically in economically developed countries and in urbanized populations. There is a growing global childhood obesity epidemic, with a large variation in secular trends across countries. Effective programs and policies are needed at global, regional and national levels to limit the problem among children.

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Author and article information

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Jose Luis Balcazar: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, USA )

ISSN (Electronic): 1932-6203

Publication date Collection: 2014

Publication date (Electronic): 22 May 2014

Volume: 9

Issue: 5

Electronic Location Identifier: e98401

Affiliations

[1 ]Department of Biochemistry & Molecular Biology II, School of Pharmacy, University of Granada, Granada, Spain

[2 ]Institute of Nutrition & Food Technology “José Mataix”, Biomedical Research Center, University of Granada, Granada, Spain

[3 ]Department of Cell Biology, School of Sciences, University of Granada, Granada, Spain

[4 ]Department of Biochemistry & Molecular Biology I, School of Sciences, University of Granada, Granada, Spain

[5 ]Hero Global Technology Center, Hero Spain, S.A., Alcantarilla, Murcia, Spain

Catalan Institute for Water Research (ICRA), Spain

Author notes

* E-mail: fontana@ 123456ugr.es

Competing Interests: Part of the research currently in progress in the authors' laboratory is funded by the company Hero Spain, S. A. through the grant #3545 managed by the Fundacion General Empresa-Universidad de Granada. Fernando Romero is employed by Hero Global Technology Center, Hero Spain, S.A. This center is part of the food company HERO, headquartered in Switzerland. There are no patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

Conceived and designed the experiments: CGLL FR AG LF. Performed the experiments: JPD FAM MJSL SMQ. Analyzed the data: JPD CGL FAM LCM AG LF. Contributed reagents/materials/analysis tools: FR. Contributed to the writing of the manuscript: JPD FAM AG LF.

[¤]

Current address: National Agency for Medicines (ANAMED), Public Health Institute, Santiago, Chile

Article

Publisher ID: PONE-D-14-11447

DOI: 10.1371/journal.pone.0098401

PMC ID: 4031175

PubMed ID: 24852284

SO-VID: ef9e9e02-3531-4306-b303-1bfb2b754a13

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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Date received : 20 March 2014

Date accepted : 16 April 2014

Page count

Pages: 9

Funding

Part of the research currently in progress in the authors' laboratory is funded by the company Hero Spain, S. A. through the grant #3545 managed by the Fundacion General Empresa-Universidad de Granada. No additional external funding was received for this study. The funders played a role in the study design, but had no role in the decision to publish or preparation of the manuscript.

Effects of Lactobacillus paracasei CNCM I-4034, Bifidobacterium breve CNCM I-4035 and Lactobacillus rhamnosus CNCM I-4036 on Hepatic Steatosis in Zucker Rats

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Most cited references 39

Banting lecture 1988. Role of insulin resistance in human disease.

Interactions between commensal intestinal bacteria and the immune system.

Worldwide trends in childhood overweight and obesity.

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