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Dietary fibre and protein do not synergistically influence insulin, metabolic or inflammatory biomarkers in young obese Göttingen Minipigs

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The effects of dietary fibre (DF) and protein on insulin response, lipidemia and inflammatory biomarkers were studied in a model experiment with juvenile obese Göttingen Minipigs. After 20 weeks feeding on a high-fat fructose-rich low-DF diet, forty-three 30-week old minipigs (31.3 ± 4.0 kg body weight) were allocated to low or high DF and protein diets for 8 weeks in a 2 × 2 factorial design. High DF contents decreased (P = 0.006) while high protein increased (P < 0.001) the daily gain. High protein contents increased fasting plasma concentrations of glucose (P = 0.008), non-esterified fatty acid (P =0.015), ghrelin (P = 0.008) and non-fasting LDL:HDL ratios (P = 0.015). High DF increased ghrelin (P = 0.036) and C-peptide levels (P = 0.011) in the non-fasting state. High protein increased the gene expression of fructose-bisphosphatase 1 in liver tissue (P = 0.043), whereas DF decreased fatty acid synthase expression in adipose tissue (P = 0.035). Interactions between DF and protein level were observed in the expression of leptin receptor in adipose tissue (P = 0.031) and of peroxisome-proliferator activated receptors-γ in muscle (P = 0.018) and adipose tissue (P = 0.004). In conclusion, high DF intake reduced weight gain and had potential benefit on beta-cell secretory function, but without effect on the lipid profile in this young obese model. High dietary protein by supplementing with whey protein did not improve insulin sensitivity or lipidemia, and combining high DF with high protein did not alleviate the risk of metabolic abnormalities.

Original languageEnglish
JournalBritish Journal of Nutrition
Pages (from-to)828-840
Number of pages13
Publication statusPublished - Apr 2021

    Research areas

  • wheat bran, whey protein, obesity, metabolic syndrom, miniature pig model, dietary fibre, metabolic syndrome, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, housekeeping genes, interferon-y, subcutaenous adipose tissue, type 2 diabetes

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