Type of diet has no major influence on inflammatory response in a Saddleback pig model

TL;DR

Adding pectin or inulin to an unhealthy diet in pigs did not reduce inflammation linked to obesity.

Contribution

This study shows fermentable carbohydrates do not resolve obesity-related inflammation in a pig model.

Findings

Faecal SCFA concentrations decreased and faecal pH increased over the feeding period.

Inflammatory markers in abdominal fat were higher than in subcutaneous fat.

Pectin or inulin supplementation did not reduce low-grade inflammation in obese pigs.

Abstract

Fermentable carbohydrates and resulting short-chain fatty acids (SCFAs) received attention via modifying potential on obesity-associated systemic low-grade inflammation. However, their effects on inflammation remain poorly understood. In this study, the anti-inflammatory properties of pectin or inulin supplementation were investigated in an atherogenic-fed pig obesity model. Pigs were divided into three atherogenic-fed groups with or without 5% pectin/inulin supplementation (AD, ADp, ADi, n = 10) and a conventional-fed group (CD, n = 10) for a 15-week feeding period. We demonstrated that faecal SCFA concentrations decreased and faecal pH increased in all groups over the feeding period (P < 0.05). SCFA concentrations were comparable between colon and faeces in all groups. Liver inflammatory-marker expressions were on average < 1 in all groups, except TNF-α (AD < CD and ADi; P < 0.01). Inflammatory-marker expressions in abdominal adipose tissue exceeded subcutaneous marker expressions in all groups. AD showed significantly lower IL-1β and CD68 mRNA levels than CD (P < 0.03). Comparing the atherogenic diet groups, the IL-1β mRNA levels were higher in ADi versus AD and ADp (P = 0.02). Our data indicated that fermentable carbohydrates added to an atherogenic diet cannot resolve low-grade adipose tissue inflammatory associated with obesity.

The online version contains supplementary material available at 10.1038/s41598-025-92420-y.

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