Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice

Abstract

Background Accumulating evidence have shown that the intestinal microbiota plays an important role in prevention of host obesity and metabolism disorders. Recent studies also demonstrate that early life is the key time for the colonization of intestinal microbes in host. However, there are few studies focusing on possible association between intestinal microbiota in the early life and metabolism in adulthood. Therefore the present study was conducted to examine whether the short term antibiotic and/or probiotic exposure in early life could affect intestinal microbes and their possible long term effects on host metabolism. Results A high-fat diet resulted in glucose and lipid metabolism disorders with higher levels of visceral fat rate, insulin-resistance indices, and leptin. Exposure to ceftriaxone in early life aggravated the negative influences of a high-fat diet on mouse physiology. Orally fed TMC3115 protected mice, especially those who had received treatment throughout the whole study, from damage due to a high-fat diet, such as increases in levels of fasting blood glucose and serum levels of insulin, leptin, and IR indices. Exposure to ceftriaxone during the first 2 weeks of life was linked to dysbiosis of the fecal microbiota with a significant decrease in the species richness and diversity. However, the influence of orally fed ceftriaxone on the fecal microbiota was limited to 12 weeks after the termination of treatment. Of note, at week 12 there were still some differences in the composition of intestinal microbiota between mice provided with high fat diet and antibiotic exposure and those only fed a high fat diet. Conclusions These results indicated that exposure to antibiotics, such as ceftriaxone, in early life may aggravate the negative influences of a high-fat diet on the physiology of the host animal. These results also suggest that the crosstalk between the host and their intestinal microbiota in early life may be more important than that in adulthood, even though the same intestinal microbes are present in adulthood.

High‐fat diet and oral infection induced type 2 diabetes and obesity development under different genetic backgrounds

“…For males on HFD, a slight aggravation was observed in the infected group and an overall improvement in the noninfected group. Almost similar results were obtained by Miao et al 55 in adult mice after HFD consumption. Interestingly, males of IL1912 on HFD show deterioration in their glucose tolerance ability in both infection conditions showing a positive ΔAUC 6–12 value, which leads to the conclusion that this line is sensitive to HFD more than a bacterial infection.…”

Lactobacillus plantarum ZJUIDS14 alleviates non-alcoholic fatty liver disease in mice in association with modulation in the gut microbiota

“…Other studies reported that in addition to lipid disorders, NAFLD patients also suffer from insulin resistance (IR) ( 23 ), playing a key role in the development of NAFLD by increasing both FFA delivery from adipose tissue and de novo lipogenesis in the liver ( 24 ). Previous studies have shown that a high-fat diet led to higher OGTT and ITT AUC values ( 25 , 26 ), which are considered the relevant parameters for scoring IR, glucose tolerance and homeostasis. In agreement with the above, the OGTT and ITT AUC values were significantly higher in the HFD group than in the NFD group.…”

Long-term use of Lacticaseibacillus paracasei N1115 from early life alleviates high-fat-diet-induced obesity and dysmetabolism in mice

“…Our previous study demonstrated that the dysbiosis of the gut microbiota in early life can aggravate the obesity, dysmetabolism, and disorders of hormone secretion induced by a HFD in mice, whereas treatment with potential probiotic strain Bifidobacterium bifidum TMC3115, even if only during early life, partly mitigated these unhealthy effects caused by the HFD (Miao et al, 2021). Long-term use of L. paracasei N1115 has been proved to reduce the release of inflammatory factors and IR in mice with NAFLD (Yao et al, 2017).…”