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Publication
Lactational metformin exposure programs offspring white adipose tissue glucose
homeostasis and resilience to metabolic stress in a sex-dependent manner.
Authors Carlson Z, Hafner H, Mulcahy M, Bullock K, Zhu A, Bridges D, Bernal-Mizrachi E,
Gregg B
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal American journal of physiology. Endocrinology and metabolism
Year 2020
Date Published 5/1/2020
Volume : Pages 318 : E600 - E612
PubMed Reference 32154743
Abstract We previously demonstrated that exposing mouse dams to metformin during
gestation results in increased beta-cell mass at birth and increased beta-cell
insulin secretion in adult male offspring. Given these favorable changes after a
gestational maternal metformin exposure, we wanted to understand the long-term
metabolic impact on offspring after exposing dams to metformin during the
postnatal window. The newborn period provides a feasible clinical window for
intervention and is important for beta-cell proliferation and metabolic tissue
development. Using a C57BL/6 model, we administered metformin to dams from the
day of birth to postnatal day 21. We monitored maternal health and offspring
growth during the lactation window, as well as adult glucose homeostasis through
in vivo testing. At necropsy we assessed pancreas and adipocyte morphology using
histological and immunofluorescent staining techniques. We found that metformin
exposure programmed male and female offspring to be leaner with a higher
proportion of small adipocytes in the gonadal white adipose tissue (GWAT). Male,
but not female, offspring had an improvement in glucose tolerance as young
adults concordant with a mild increase in insulin secretion in response to
glucose in vivo. These data demonstrate long-term metabolic programming of
offspring associated with maternal exposure to metformin during lactation.





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