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      Rice Endosperm Protein Administration to Juvenile Mice Regulates Gut Microbiota and Suppresses the Development of High-Fat Diet-Induced Obesity and Related Disorders in Adulthood

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          Abstract

          Obesity and related disorders, which are increasing in adults worldwide, are closely linked to childhood diet and are associated with chronic inflammation. Rice endosperm protein (REP) intake during adulthood has been reported to improve lipid metabolism and suppress the progression of diabetic kidney disease in animal models. However, the effects of REP intake during childhood on adulthood health are unclear. Therefore, we used a mouse model to experimentally investigate the preconditioning effects of REP intake during childhood on the development of obesity and related disorders in adulthood. Male C57BL/6J mice were pair-fed a normal-fat diet containing casein or REP during the juvenile period and then a high-fat diet (HFD) containing casein or REP during adulthood. Mice fed REP during the juvenile period showed better body weight, blood pressure, serum lipid profiles, lipopolysaccharide (LPS)-binding protein levels, and glucose tolerance in adulthood than those fed casein during the juvenile period. HFD-induced renal tubulo-glomerular alterations and hepatic microvesicular steatosis were less evident in REP-fed mice than in casein-fed ones. REP intake during the juvenile period improved HFD-induced dysbiosis (i.e., Escherichia genus proliferation and reduced gut microbiota diversity), thereby suppressing endotoxin-related chronic inflammation. Indeed, REP-derived peptides showed antibacterial activity against Escherichia coli, a major producer of LPS. In conclusion, REP supplementation during the juvenile period may regulate the gut microbiota and thus suppress the development of obesity and related disorders in adulthood in mice.

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          The medical care costs of obesity: an instrumental variables approach.

          This paper is the first to use the method of instrumental variables (IV) to estimate the impact of obesity on medical costs in order to address the endogeneity of weight and to reduce the bias from reporting error in weight. Models are estimated using restricted-use data from the Medical Expenditure Panel Survey for 2000-2005. The IV model, which exploits genetic variation in weight as a natural experiment, yields estimates of the impact of obesity on medical costs that are considerably higher than the estimates reported in the previous literature. For example, obesity is associated with $656 higher annual medical care costs, but the IV results indicate that obesity raises annual medical costs by $2741 (in 2005 dollars). These results imply that the previous literature has underestimated the medical costs of obesity, resulting in underestimates of the economic rationale for government intervention to reduce obesity-related externalities. Copyright © 2011 Elsevier B.V. All rights reserved.
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            Interaction between obesity and the gut microbiota: relevance in nutrition.

            This review examines mechanisms by which the bacteria present in the gut interact with nutrients and host biology to affect the risk of obesity and associated disorders, including diabetes, inflammation, and liver diseases. The bacterial metabolism of nutrients in the gut is able to drive the release of bioactive compounds (including short-chain fatty acids or lipid metabolites), which interact with host cellular targets to control energy metabolism and immunity. Animal and human data demonstrate that phylogenic changes occur in the microbiota composition in obese versus lean individuals; they suggest that the count of specific bacteria is inversely related to fat mass development, diabetes, and/or the low levels of inflammation associated with obesity. The prebiotic and probiotic approaches are presented as interesting research tools to counteract the drop in target bacteria and thereby to estimate their relevance in the improvement of host metabolism.
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              Association of adolescent obesity with risk of severe obesity in adulthood.

              Although the prevalence of obesity has increased in recent years, individuals who are obese early in life have not been studied over time to determine whether they develop severe obesity in adulthood, thus limiting effective interventions to reduce severe obesity incidence and its potentially life-threatening associated conditions. To determine incidence and risk of severe obesity in adulthood by adolescent weight status. A cohort of 8834 individuals aged 12 to 21 years enrolled in 1996 in wave II of the US National Longitudinal Study of Adolescent Health, followed up into adulthood (ages 18-27 years during wave III [2001-2002] and ages 24-33 years during wave IV [2007-2009]). Height and weight were obtained via anthropometry and surveys administered in study participants' homes using standardized procedures. New cases of adult-onset severe obesity were calculated by sex, race/ethnicity, and adolescent weight status. Sex-stratified, discrete time hazard models estimated the net effect of adolescent obesity (aged <20 years; body mass index [BMI] ≥95th percentile of the sex-specific BMI-for-age growth chart or BMI ≥30.0) on risk of severe obesity incidence in adulthood (aged ≥20 years; BMI ≥40.0), adjusting for race/ethnicity and age and weighted for national representation. In 1996, 79 (1.0%; 95% confidence interval [CI], 0.7%-1.4%) adolescents were severely obese; 60 (70.5%; 95% CI, 57.2%-83.9%) remained severely obese in adulthood. By 2009, 703 (7.9%; 95% CI, 7.4%-8.5%) non-severely obese adolescents had become severely obese in adulthood, with the highest rates for non-Hispanic black women. Obese adolescents were significantly more likely to develop severe obesity in young adulthood than normal-weight or overweight adolescents (hazard ratio, 16.0; 95% CI, 12.4-20.5). In this cohort, obesity in adolescence was significantly associated with increased risk of incident severe obesity in adulthood, with variations by sex and race/ethnicity.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                02 December 2019
                December 2019
                : 11
                : 12
                : 2919
                Affiliations
                [1 ]Department of Applied Molecular Medicine, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata 951-8510, Japan; n14b140g@ 123456mail.cc.niigata-u.ac.jp (Y.H.); kuwahara.s@ 123456shc.usp.ac.jp (S.K.); sawako-g@ 123456med.niigata-u.ac.jp (S.G.); djkozytoba52@ 123456gmail.com (K.T.)
                [2 ]Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata 951-8510, Japan; ryoheik@ 123456med.niigata-u.ac.jp (R.K.); naritai@ 123456med.niigata-u.ac.jp (I.N.)
                [3 ]Department of Clinical Nutrition Science, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata 951-8510, Japan; hkabasawa@ 123456med.niigata-u.ac.jp
                [4 ]Clinical and Translational Research Center, Niigata University Medical and Dental Hospital, 1-754 Asahimachi-dori, Chuo-ku, Niigata 951-8520, Japan; ta-tnk@ 123456med.niigata-u.ac.jp (T.T.); nktmr@ 123456m12.alpha-net.ne.jp (N.K.)
                [5 ]Division of Bioinformatics, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata 951-8510, Japan; takihara@ 123456med.niigata-u.ac.jp (H.T.); okd@ 123456med.niigata-u.ac.jp (S.O.)
                [6 ]Department of Materials Science and Technology, Niigata University, 2-8050 Ikarashi, Nishi-ku, Niigata 950-2181, Japan; mtanig@ 123456eng.niigata-u.ac.jp
                [7 ]Rice Research Center, Kameda Seika Co. Ltd., 3-1-1 Kameda-kogyodanchi, Kounan-ku, Niigata 950-0198, Japan; h_arao@ 123456sk.kameda.co.jp
                Author notes
                [* ]Correspondence: hoso9582@ 123456med.niigata-u.ac.jp (M.H.); akisaito@ 123456med.niigata-u.ac.jp (A.S.); Tel.: +81-25-368-9312 (M.H.); +81-25-227-0915 (A.S.)
                Author information
                https://orcid.org/0000-0002-2750-735X
                https://orcid.org/0000-0002-6185-0346
                https://orcid.org/0000-0002-8403-5782
                https://orcid.org/0000-0002-7704-8104
                Article
                nutrients-11-02919
                10.3390/nu11122919
                6950226
                31810329
                1434beab-2a57-419b-b35d-45aad381e8ca
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 06 November 2019
                : 29 November 2019
                Categories
                Article

                Nutrition & Dietetics
                childhood nutrition,gut microbiota,kidney disease,metabolic syndrome,obesity,rice protein

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