A new oral model of free fatty acid kinetics to assess lipolysis in subjects with and without type 2 diabetes.
glucose metabolism
identifiability
insulin sensitivity
parameter estimation
prediabetes
Journal
American journal of physiology. Endocrinology and metabolism
ISSN: 1522-1555
Titre abrégé: Am J Physiol Endocrinol Metab
Pays: United States
ID NLM: 100901226
Informations de publication
Date de publication:
01 08 2023
01 08 2023
Historique:
pmc-release:
01
08
2024
medline:
21
7
2023
pubmed:
28
6
2023
entrez:
28
6
2023
Statut:
ppublish
Résumé
Assessing free fatty acids (FFAs) kinetics and the role of insulin and glucose on FFA lipolysis and disposal may improve our understanding of the pathogenesis of type 2 diabetes (T2D). Some models have been proposed to describe FFA kinetics during an intravenous glucose tolerance test and only one during an oral glucose tolerance test. Here, we propose a model of FFA kinetics during a meal tolerance test and use it to assess possible differences in postprandial lipolysis in individuals with type 2 diabetes (T2D) and individuals with obesity without type 2 diabetes (ND). We studied 18 obese ND and 16 T2D undergoing three meal tolerance tests (MTT) on three occasions (breakfast, lunch, and dinner). We used plasma glucose, insulin, and FFA concentrations collected at breakfast to test a battery of models and selected the best one based on physiological plausibility, ability to fit the data, precision of parameter estimates, and the Akaike parsimony criterion. The best model assumes that the postprandial suppression of FFA lipolysis is proportional to the above basal insulin, while FFA disposal is proportional to FFA concentration. It was used to compare FFA kinetics in ND and T2D along the day. The maximum lipolysis suppression occurred significantly earlier in ND than T2D (39 ± 6 min vs. 102 ± 13 min, 36 ± 4 min vs. 78 ± 11 min, and 38 ± 6 min vs. 84 ± 13 min,
Identifiants
pubmed: 37378622
doi: 10.1152/ajpendo.00091.2023
pmc: PMC10393336
doi:
Substances chimiques
Fatty Acids, Nonesterified
0
Blood Glucose
0
Insulin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
E163-E170Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK056336
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK029953
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK085516
Pays : United States
Organisme : NIDDK NIH HHS
ID : R37 DK029953
Pays : United States
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