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Intestinal gluconeo...
Intestinal gluconeogenesis is downregulated in pediatric patients with celiac disease
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- Karlson, Olof, 1996 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Department of Laboratory Medicine,Sahlgrenska Academy
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- Arnell, H. (author)
- Karolinska Institutet,Karolinska Institute,Karolinska University Hospital
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- Gudjonsdottir, A. H. (author)
- Queen Silvia Children’s Hospital
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- Agardh, Daniel (author)
- Lund University,Lunds universitet,Celiaki och diabetes,Forskargrupper vid Lunds universitet,Celiac Disease and Diabetes Unit,Lund University Research Groups
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- Torinsson Naluai, Åsa, 1968 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Department of Laboratory Medicine,Sahlgrenska Academy
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(creator_code:org_t)
- 2022-11-11
- 2022
- English.
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In: Bmc Medicine. - : Springer Science and Business Media LLC. - 1741-7015. ; 20:1
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Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Pediatrik (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Pediatrics (hsv//eng)
Keyword
- Celiac disease
- Gluten
- intestinal gluconeogenesis
- Non-alcoholic fatty
- liver disease
- rat small-intestine
- glucose-6-phosphatase
- expression
- diagnosis
- gene
- pcr
- General & Internal Medicine
- Non-alcoholic fatty liver disease
Publication and Content Type
- ref (subject category)
- art (subject category)
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