Plasma insulin is required for the increase in plasma angiopoietin-like protein 8 in response to nutrient ingestion.


Journal

Diabetes/metabolism research and reviews
ISSN: 1520-7560
Titre abrégé: Diabetes Metab Res Rev
Pays: England
ID NLM: 100883450

Informations de publication

Date de publication:
09 2023
Historique:
revised: 28 02 2023
received: 16 10 2022
accepted: 17 03 2023
medline: 4 9 2023
pubmed: 30 3 2023
entrez: 29 3 2023
Statut: ppublish

Résumé

Plasma levels of angiopoietin-like protein 8 (ANGPTL8) are regulated by feeding and they increase following glucose ingestion. Because both plasma glucose and insulin increase following food ingestion, we aimed to determine whether the increase in plasma insulin and glucose or both are responsible for the increase in ANGPTL8 levels. ANGPTL8 levels were measured in 30 subjects, 14 with impaired fasting glucose (IFG), and 16 with normal fasting glucose (NFG); the subjects received 75g glucose oral Glucose tolerance test (OGTT), multistep euglycaemic hyperinsulinemic clamp and hyperglycaemic clamp with pancreatic clamp. Subjects with IFG had significantly higher ANGPTL8 than NGT subjects during the fasting state (p < 0.05). During the OGTT, plasma ANGPTL8 concentration increased by 62% above the fasting level (p < 0.0001), and the increase above fasting in ANGPTL8 levels was similar in NFG and IFG individuals. During the multistep insulin clamp, there was a dose-dependent increase in plasma ANGPTL8 concentration. During the 2-step hyperglycaemic clamp, the rise in plasma glucose concentration failed to cause any change in the plasma ANGPTL8 concentration from baseline. In response to nutrient ingestion, ANGPTL8 level increased due to increased plasma insulin concentration, not to the rise in plasma glucose. The incremental increase above baseline in plasma ANGLPTL8 during OGTT was comparable between people with normal glucose tolerance and IFG.

Sections du résumé

BACKGROUND
Plasma levels of angiopoietin-like protein 8 (ANGPTL8) are regulated by feeding and they increase following glucose ingestion. Because both plasma glucose and insulin increase following food ingestion, we aimed to determine whether the increase in plasma insulin and glucose or both are responsible for the increase in ANGPTL8 levels.
METHODS
ANGPTL8 levels were measured in 30 subjects, 14 with impaired fasting glucose (IFG), and 16 with normal fasting glucose (NFG); the subjects received 75g glucose oral Glucose tolerance test (OGTT), multistep euglycaemic hyperinsulinemic clamp and hyperglycaemic clamp with pancreatic clamp.
RESULTS
Subjects with IFG had significantly higher ANGPTL8 than NGT subjects during the fasting state (p < 0.05). During the OGTT, plasma ANGPTL8 concentration increased by 62% above the fasting level (p < 0.0001), and the increase above fasting in ANGPTL8 levels was similar in NFG and IFG individuals. During the multistep insulin clamp, there was a dose-dependent increase in plasma ANGPTL8 concentration. During the 2-step hyperglycaemic clamp, the rise in plasma glucose concentration failed to cause any change in the plasma ANGPTL8 concentration from baseline.
CONCLUSIONS
In response to nutrient ingestion, ANGPTL8 level increased due to increased plasma insulin concentration, not to the rise in plasma glucose. The incremental increase above baseline in plasma ANGLPTL8 during OGTT was comparable between people with normal glucose tolerance and IFG.

Identifiants

pubmed: 36988137
doi: 10.1002/dmrr.3643
doi:

Substances chimiques

Blood Glucose 0
Angiopoietin-Like Protein 8 0
Insulin 0
Glucose IY9XDZ35W2
Insulin, Regular, Human 0
ANGPTL8 protein, human 0
Peptide Hormones 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e3643

Informations de copyright

© 2023 John Wiley & Sons Ltd.

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Auteurs

Mohamed Abu-Farha (M)

Biochemistry and Molecular Biology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.

Mariam Alatrach (M)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

Jehad Abubaker (J)

Biochemistry and Molecular Biology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.

Irina Al-Khairi (I)

Biochemistry and Molecular Biology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.

Preethi Cherian (P)

Biochemistry and Molecular Biology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.

Krisitn Agyin (K)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

Siham Abdelgani (S)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

Luke Norton (L)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

John Adams (J)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

Dalal Al-Saeed (D)

Dasman Diabetes Institute, Kuwait City, Kuwait.

Ebaa Al-Ozairi (E)

Dasman Diabetes Institute, Kuwait City, Kuwait.

Ralph A DeFronzo (RA)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

Fahd Al-Mulla (F)

Dasman Diabetes Institute, Kuwait City, Kuwait.

Muhammad Abdul-Ghani (M)

Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas, USA.

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