Early Life Nutrition and Metabolic Syndrome

Abstract BackgroundLow-dose antibiotic contamination in animal food is still a severe food safety problem worldwide. Penicillin is one of the main classes of antibiotics being detected in food. Previous studies have shown that transient exposure of low-dose penicillin (LDP) during early life resulted in metabolic syndrome (MetS) in mice. However, the underlying mechanism(s) and efficient approaches to counteracting this are largely unknown.MethodsWild-type (WT) or secretory IgA (SIgA)-deficient (Pigr-/-) C57BL/6 mice were exposed to LDP or not from several days before birth to 30 d of age. Five times of FMT or probiotics (a mixture of Lactobacillus bulgaricus and L. rhamnosus GG) treatments were applied to parts of these LDP-treated mice from 12 d to 28 d of life. Bacterial composition from different regions (mucosa and lumen) of the colon and ileum were analyzed through 16S rDNA sequencing. Intestinal IgA response was analyzed. Multiple parameters related to MetS were also determined. In addition, germ-free animals and in vitro tissue culture were also used to determine the correlations between LDP, gut microbiota (GM) and intestinal IgA response.ResultsLDP disturbed the intestinal bacterial composition, especially for ileal mucosa, the main inductive and effective sites of IgA response, in 30-d-old mice. The alteration of early GM resulted in a persistent inhibition of the intestinal IgA response, leading to a constant reduction of fecal and caecal SIgA levels throughout the 25-week experiment, which is early life-dependent, as transfer of LDP-GM to 30 d germ-free mice only resulted in a transient reduction in fecal SIgA. LDP-induced reduction in SIgA led to a decrease in IgA+ bacteria and a dysbiosis in the ileal mucosal samples of 25 week wild-type but not Pigr-/- mice. Moreover, LDP also resulted in increases in ileal bacterial encroachment and adipose inflammation, along with an enhancement of diet-induced MetS in an intestinal SIgA-dependent manner. Furthermore, several times of FMT or probiotic treatments during LDP treatment are efficient to fully (for FMT) or partially (for probiotics) counteract the LDP-effect on both GM and metabolism.ConclusionsEarly-life LDP-induced enhancement of diet-induced MetS is mediated by intestinal SIgA, which could be (partially) restored by FMT or probiotics treatment.

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Victims of Chinese famine in early life have increased risk of metabolic syndrome in adulthood

Nutrition ◽

10.1016/j.nut.2017.12.013 ◽

2018 ◽

Vol 53 ◽

pp. 20-25 ◽

Cited By ~ 8

Author(s):

Caizheng Yu ◽

Jing Wang ◽

Fei Wang ◽

Xu Han ◽

Hua Hu ◽

...

Keyword(s):

Metabolic Syndrome ◽

Early Life ◽

Increased Risk

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Metabolic Syndrome Due to Early Life Nutritional Modifications

Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome ◽

10.1201/9781420043792-10 ◽

2007 ◽

pp. 69-92

Keyword(s):

Metabolic Syndrome ◽

Early Life

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Interplay between early-life malnutrition, epigenetic modulation of the immune function and liver diseases

Nutrition Research Reviews ◽

10.1017/s0954422418000239 ◽

2019 ◽

Vol 32 (1) ◽

pp. 128-145 ◽

Cited By ~ 4

Author(s):

Sabrina Campisano ◽

Anabela La Colla ◽

Stella M. Echarte ◽

Andrea N. Chisari

Keyword(s):

Metabolic Syndrome ◽

Immune System ◽

Environmental Factors ◽

Early Life ◽

Critical Role ◽

Later Life ◽

Covalent Modification ◽

Alcoholic Fatty Liver ◽

The Metabolic Syndrome ◽

Epigenetic Modulation

AbstractEarly-life nutrition plays a critical role in fetal growth and development. Food intake absence and excess are the two main types of energy malnutrition that predispose to the appearance of diseases in adulthood, according to the hypothesis of ‘developmental origins of health and disease’. Epidemiological data have shown an association between early-life malnutrition and the metabolic syndrome in later life. Evidence has also demonstrated that nutrition during this period of life can affect the development of the immune system through epigenetic mechanisms. Thus, epigenetics has an essential role in the complex interplay between environmental factors and genetics. Altogether, this leads to the inflammatory response that is commonly seen in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome. In conjunction, DNA methylation, covalent modification of histones and the expression of non-coding RNA are the epigenetic phenomena that affect inflammatory processes in the context of NAFLD. Here, we highlight current understanding of the mechanisms underlying developmental programming of NAFLD linked to epigenetic modulation of the immune system and environmental factors, such as malnutrition.

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Association of Exposure to Chinese Famine in Early Life with the Risk of Metabolic Syndrome in Adulthood

Annals of Nutrition and Metabolism ◽

10.1159/000507356 ◽

2020 ◽

Vol 76 (2) ◽

pp. 140-146 ◽

Cited By ~ 1

Author(s):

Yue Peng ◽

Miaomiao Hai ◽

Pengcheng Li ◽

Yongjie Chen

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Early Childhood ◽

Early Life ◽

Lower Risk ◽

Late Childhood ◽

Fetal Life ◽

Childhood Exposure ◽

Study Results ◽

Famine Exposure

Objective: To explore the association of famine exposure in early life with the risk of metabolic syndrome (MS) in the Chinese adults. Methods: Data were obtained from the wave 2009 of the China Health and Nutrition Survey. MS was identified when 3 or more of the following components happened: (1) waist circumference >90 cm in males or >85 cm in females; (2) fasting glucose ≥6.1 mmol/L; (3) systolic blood pressure ≥130 mm Hg/diabolic blood pressure ≥85 mm Hg; (4) fasting triglyceride ≥1.70 mmol/L; and (5) high-density lipids cholesterol <1.04 mmol/L. All participants were divided into 5 groups: no exposure, born after 1961; fetal life exposure, between 1959 and 1961; early childhood exposure, between 1956 and 1958; mid-childhood exposure, between 1953 and 1955; and late childhood exposure, between 1949 and 1952. A total of 2,080 subjects were included in this study. Results: In rural, famine exposure in fetal life and early childhood was associated with the lower risk of MS (p = 0.0491 and 0.0245; OR 0.583 and 0.703; and OR, 95% CI 0.341–0.998 and 0.517–0.956, respectively). But famine exposure in late childhood was associated with the higher risk of MS (p = 0.0140; OR 3.096; and OR, 95% CI 1.257–7.625). Famine exposure in early childhood was associated with the lower risk of MS (p = 0.0120; OR 0.633; and OR, 95% CI 0.443–0.904) in males. Conclusions: Famine exposure in mid- and late-childhood was associated with the higher risk of MS, especially in rural, males, and severe famine areas.

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