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. 2022 Nov 11;20(1):440.

doi: 10.1186/s12916-022-02635-3.

Intestinal gluconeogenesis is downregulated in pediatric patients with celiac disease

Olof Karlson  ¹ , Henrik Arnell  ^{2   3} , Audur H Gudjonsdottir  ⁴ , Daniel Agardh  ⁵ , Åsa Torinsson Naluai  ⁶

Affiliations

• PMID: 36369023
• PMCID: PMC9652951
• DOI: 10.1186/s12916-022-02635-3

Abstract

Background: Untreated celiac disease (CD) patients have increased levels of blood glutamine and a lower duodenal expression of glutaminase (GLS). Intestinal gluconeogenesis (IGN) is a process through which glutamine is turned into glucose in the small intestine, for which GLS is crucial. Animal studies suggest impaired IGN may have long-term effects on metabolic control and be associated with the development of type 2 diabetes and non-alcoholic fatty liver disease (NAFLD). The aim of this study was to thoroughly investigate IGN at the gene expression level in children with untreated celiac disease.

Methods: Quantitative polymerase chain reaction (qPCR) was used to quantify the expression of 11 target genes related to IGN using the delta-delta Ct method with three reference genes (GUSB, IPO8, and YWHAZ) in duodenal biopsies collected from 84 children with untreated celiac disease and 58 disease controls.

Results: Significantly lower expression of nine target genes involved in IGN was seen in duodenal biopsies from CD patients compared with controls: FBP1, G6PC, GLS, GPT1, PCK1, PPARGC1A, SLC2A2, SLC5A1, and SLC6A19. No significant difference in the expression was observed for G6PC3 or GOT1.

Conclusions: Children with untreated celiac disease have lower expression of genes important for IGN. Further studies are warranted to disentangle whether this is a consequence of intestinal inflammation or due to an impaired metabolic pathway shared with other chronic metabolic diseases. Impaired IGN could be a mechanism behind the increased risk of NAFLD seen in CD patients.

Keywords: Celiac disease; Gluten; Non-alcoholic fatty liver disease; intestinal gluconeogenesis.

© 2022. The Author(s).

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Conflict of interest statement

The authors declare that they have no competing interests.