Adverse Metabolic Phenotypes in Parenterally Fed Neonatal Pigs Do Not Persist into Adolescence

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Background
Nutrition during fetal and neonatal life is an important determinant for the risk of adult-onset diseases, especially type 2 diabetes and obesity.

Objectives
We aimed to determine whether total parenteral nutrition (TPN) compared with enteral formula feeding [enteral nutrition (EN)] in term piglets during the first 2 wk after birth would increase the long-term (5-mo) development of metabolic syndrome phenotypes with adverse glucose homeostasis, fatty liver disease, and obesity.

Methods
Neonatal female pigs were administered TPN (n = 12) or fed enterally with a liquid enteral milk-replacer formula (EN, n = 12) for 14 d. After transitioning TPN pigs to enteral feeding of liquid formula (days 15–26), both groups were adapted to a solid high-fat diet (30% of the total diet) and sucrose (20% of the total diet) diet (days 27–33), which was fed until the end of the study (140 d). Body composition was measured by dual-energy X-ray absorptiometry at 14, 45, and 140 d. Serum biochemistry and glucose-insulin values (after a fasting intravenous glucose tolerance test) were obtained at 140 d. Liver and muscle were analyzed for insulin receptor signaling and triglycerides.

Results
Body weight was similar, but percent fat was higher, whereas percent lean and bone mineral density were lower in TPN than in EN pigs (P < 0.01) at 45 d of age but not at 140 d. At 140 d, there were no differences in serum markers of liver injury or lipidemia. Intravenous glucose tolerance test at 140 d showed a lower (P < 0.05) AUC for both glucose and insulin in TPN than in EN pigs, but the ratio of AUCs of insulin and glucose was not different between groups.

Conclusions
Administration of TPN during the neonatal period increased adipose deposition that transiently persisted in early adolescence when challenged with a high-fat diet but was not sustained or manifested as glucose intolerance.
OriginalsprogEngelsk
TidsskriftJournal of Nutrition
Vol/bind154
Udgave nummer2
Sider (fra-til)638-647
Antal sider10
ISSN0022-3166
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
This project was supported in part by federal funds from the USDA , Agricultural Research Service under cooperative agreement number 3092-51000-060-01, the American Society for Parenteral and Enteral Nutrition Rhoads Research Foundation (BS), and grants from the NIH grant DK-094616 (DGB) and HD-085573 (TAD), and the Texas Medical Center Digestive Diseases Center ( NIH grant P30 DK-56338). SKF was supported by T32 DK007664.

Publisher Copyright:
© 2024

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