Tag: low-fat diets

A study I contributed to was published!

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A study was recently published, led by Dr. Huawei Zeng, USDA Animal Research Station, on gut health, nutrition, and gut microbiota! I contributed analysis and interpretation for the gut community data, and though I appear as last author on this publication, it is truly because I contributed the least and not because I was administrative lead or the lead PI. I have worked with Dr. Zeng for several years, although we have never met in person,

Dr. Zeng’s presentation of this project can be found here: Adequacy of calcium and vitamin D enriches probiotic bacteria and reduces dysbiotic Parasutterela bacteria and inflammation in the colon of C57BL/6 mice fed a Western-style diet

Zeng, H., Safratowich, B.D., Liu, Z., Bukowski, , M.R., Ishaq, S.L. 2021. Adequacy of calcium and vitamin D reduces inflammation, β-catenin signaling, and dysbiotic Parasutterella bacteria in the colon of C57BL/6 mice fed a Western-style diet. Journal of Nutritional Biochemistry. In press.

Abstract

Adoption of an obesogenic diet low in calcium and vitamin D (CaD) leads to increased obesity, colonic inflammation, and cancer. However, the underlying mechanisms remain to be elucidated. We tested the hypothesis that CaD supplementation (from inadequacy to adequacy) may reduce colonic inflammation, oncogenic signaling, and dysbiosis in the colon of C57BL/6 mice fed a Western diet. Male C57/BL6 mice (4-week old) were assigned to 3 dietary groups for 36 weeks: (1) AIN76A as a control diet (AIN); (2) a defined rodent “new Western diet” (NWD); or (3) NWD with CaD supplementation (NWD/CaD). Compared to the AIN, mice receiving the NWD or NWD/CaD exhibited more than 0.2-fold increase in the levels of plasma leptin, tumor necrosis factor α (TNF-α) and body weight. The levels of plasma interleukin 6 (IL-6), inflammatory cell infiltration, and β-catenin/Ki67 protein (oncogenic signaling) were increased more than 0.8-fold in the NWD (but not NWD/CaD) group compared to the AIN group. Consistent with the inflammatory phenotype, colonic secondary bile acid (BA, inflammatory bacterial metabolite) levels increased more than 0.4-fold in the NWD group compared to the NWD/CaD and AIN groups. Furthermore, the abundance of colonic Proteobacteria (e.g., Parasutterela), considered signatures of dysbiosis, was increased more than 4-fold; and the α diversity of colonic bacterial species, indicative of health, was decreased by 30% in the NWD group compared to the AIN and NWD/CaD groups. Collectively, CaD adequacy reduces colonic inflammation, β-catenin oncogenic signaling, secondary BAs, and bacterial dysbiosis in mice fed with a Western diet.

This is part of a multi-year collaboration, with previous publications:

  • Zeng, H., Ishaq, S.L., Liu, Z., Bukowski, M.R. 2017. Colonic aberrant crypt formation accompanies an increase of opportunistic pathogenic bacteria in C57BL/6 mice fed a high-fat diet. Journal of Nutritional Biochemistry 54:18-27. Impact 4.418. Article.
  • Zeng, H., Ishaq, S.L., Zhao, F-Q., Wright, A-D.G. 2016. Colonic inflammation accompanies an increase of b-catenin signaling Lachnospiraceae/Streptococcaceae in the hind-gut of high-fat diet-fed mice. Journal of Nutritional Biochemistry 25:30-36. Impact 4.518. Article

Manuscript published on the effect of low/high fat diets on health and intestinal bacteria

sueishaqlabLeave a comment

Several years ago, during my Ph.D. at the University of Vermont, I provided wet-lab and DNA sequence analysis work for a project investigating the health effects of a low or high fat diet on mice with Dr. Huawei Zeng of the USDA Agricultural Research Service.  It was just recently published in the Journal of Nutritional Biochemistry!

Abstract

Consumption of an obesigenic/high-fat diet (HFD) is associated with a high colon cancer risk and may alter the gut microbiota. To test the hypothesis that long-term high-fat (HF) feeding accelerates inflammatory process and changes gut microbiome composition, C57BL/6 mice were fed HFD (45% energy) or a low-fat (LF) diet (10% energy) for 36 weeks. At the end of the study, body weights in the HF group were 35% greater than those in the LF group. These changes were associated with dramatic increases in body fat composition, inflammatory cell infiltration, inducible nitric oxide synthase protein concentration and cell proliferation marker (Ki67) in ileum and colon. Similarly, β-catenin expression was increased in colon (but not ileum). Consistent with gut inflammation phenotype, we also found that plasma leptin, interleukin 6 and tumor necrosis factor α concentrations were also elevated in mice fed the HFD, indicative of chronic inflammation. Fecal DNA was extracted and the V1–V3 hypervariable region of the microbial 16S rRNA gene was amplified using primers suitable for 454 pyrosequencing. Compared to the LF group, the HF group had high proportions of bacteria from the family Lachnospiraceae/Streptococcaceae, which is known to be involved in the development of metabolic disorders, diabetes and colon cancer. Taken together, our data demonstrate, for the first time, that long-term HF consumption not only increases inflammatory status but also accompanies an increase of colonic β-catenin signaling and Lachnospiraceae/Streptococcaceae bacteria in the hind gut of C57BL/6 mice.