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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Aging Reduces Insulin Clearance in Mice

Full text
Author(s):
Marmentini, Carine [1] ; Soares, Gabriela M. [1] ; Bronczek, Gabriela A. [1] ; Piovan, Silvano [2] ; Mareze-Costa, Cecilia E. [2] ; Carneiro, Everardo M. [1] ; Boschero, Antonio C. [1] ; Kurauti, Mirian A. [1, 2]
Total Authors: 8
Affiliation:
[1] Univ Campinas UNICAMP, Obes & Comorbid Res Ctr OCRC, Lab Endocrine Pancreas & Metab, Campinas - Brazil
[2] State Univ Maringa UEM, Biol Sci Ctr, Dept Physiol Sci, Maringa, Parana - Brazil
Total Affiliations: 2
Document type: Journal article
Source: FRONTIERS IN ENDOCRINOLOGY; v. 12, MAY 12 2021.
Web of Science Citations: 0
Abstract

Hyperinsulinemia is frequently associated with aging and may cause insulin resistance in elderly. Since insulin secretion and clearance decline with age, hyperinsulinemia seems to be maintained, primarily, due to a decrease in the insulin clearance. To investigate these aging effects, 3- and 18-month-old male C57BL/6 mice were subjected to intraperitoneal glucose and insulin tolerance tests (ipGTT and ipITT) and, during the ipGTT, plasma c-peptide and insulin were measure to evaluate in vivo insulin clearance. Glucose-stimulated insulin secretion in isolated pancreatic islets was also assessed, and liver samples were collected for molecular analyses (western blot). Although insulin sensitivity was not altered in the old mice, glucose tolerance, paradoxically, seems to be increased, accompanied by higher plasma insulin, during ipGTT. While insulin secretion did not increase, insulin clearance was reduced in the old mice, as suggested by the lower c-peptide:insulin ratio, observed during ipGTT. Carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) and insulin-degrading enzyme (IDE), as well as the activity of this enzyme, were reduced in the liver of old mice, justifying the decreased insulin clearance observed in these mice. Therefore, loss of hepatic CEACAM1 and IDE function may be directly related to the decline in insulin clearance during aging. (AU)

FAPESP's process: 15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass
Grantee:Antonio Carlos Boschiero
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 18/24368-0 - Action of PPAR gamma (Peroxisome Proliferator Activated Receptor gamma) and AMPK (AMP-activated protein kinase) on the expression of IDE (Insulin Degrading Enzyme) in pancreatic beta cells
Grantee:Carine Marmentini
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 17/06475-1 - Effect of physical exercise on modulation of peroxisome proliferator-activated receptor ³ (PPAR³) and insulin-degrading enzyme (IDE) in the pancreatic islet of mice
Grantee:Mirian Ayumi Kurauti
Support Opportunities: Scholarships in Brazil - Post-Doctoral