Rat maternal diabetes impairs pancreatic β-cell function in the offspring
Abstract
It has been shown that maternal diabetes increases the risk for obesity, glucose intolerance, and Type 2 diabetes mellitus in the adult life of the offspring. Mechanisms for these effects on the offspring are not well understood, and little information is available to reveal the mechanisms. We studied the effect of maternal diabetes on beta-cell function in the offspring of streptozotocin (STZ)-induced diabetic rat mothers (STZ-offspring). STZ-offspring did not become glucose intolerant up to 15 wk of age. At this age, however, insulin secretion was significantly impaired, as measured by in vivo and in vitro studies. Consistent with these changes, islet glucose metabolism and some important glucose metabolic enzyme activities were reduced. No significant changes were found in islet morphological analysis. These data indicate that beta-cell function is impaired in adult STZ-offspring; these changes may contribute to the development of type 2 diabetes mellitus in adulthood.
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Despite maternal plasma glucose levels exceeding the clinical definition of gestational diabetes mellitus, 80-day-old Wistar rat offspring and 15-week-old Sprague-Dawley rat offspring remained glucose tolerant with normal islet morphology and retained similar plasma glucose and insulin levels as controls.
“Despite maternal plasma glucose levels exceeding the clinical definition of GDM, 80-day-old Wistar rat offspring [90] and 15-week-old Sprague-Dawley rat offspring [92] remained glucose tolerant with normal islet morphology [92] and retained similar plasma glucose and insulin levels as controls [90].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [92]
Streptozotocin has been used to cause β-cell destruction in order to produce maternal insulin deficiency and hyperglycemia, though this more closely approximates type 1 diabetes.
“To model diabetes during pregnancy, streptozotocin (STZ) has been used to cause β-cell destruction in order to produce maternal insulin deficiency and hyperglycemia, though this more closely approximates type 1 diabetes [90,91,92].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [92]
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Bouret, S., Levin, B. E., & Ozanne, S. E. (2015) · Physiological Reviews · doi:10.1152/physrev.00007.2014 · Cited by 157 · see citing works
Early-Life Origins of Type 2 Diabetes: Fetal Programming of the Beta-Cell Mass
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Gestational hyperglycemia reprograms cardiac gene expression in rat offspring
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- Authors
- Han, J., Xu, J., Long, Y. S., Epstein, P. N., & Liu, Y. Q.
- Affiliations
- University of Louisville (US)
- ORCID
- Epstein, Paul N.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2007-07
- Volume
- 293
- Issue
- 1
- Pages
- E228-E236
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2102128931
- Cited by
- 45
- References
- 5
- Citations by year
- 2024: 2 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 5 · 2018: 4 · 2017: 1 · 2016: 4 · 2014: 4 · 2013: 2 · 2012: 3
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01dk077624-02)
- National Heart, Lung, and Blood Institute (HL075080, R01HL075080)
- National Institute of Diabetes and Digestive and Kidney Diseases (1 R01 DK077624-01)
- National Institute of Dental and Craniofacial Research (P20 RR/DE17702)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- maternal diabetes, beta-cell function, offspring, streptozotocin-induced diabetes, insulin secretion, islet glucose metabolism, type 2 diabetes, impaired glucose tolerance, islet morphology, rat model
- MeSH terms
- Insulin Secretion, Animals, Animals, Newborn, Birth Weight, Blood Glucose, Body Weight, Diabetes Mellitus, Experimental, Female, Glucose, Insulin, Islets of Langerhans, Male, Pregnancy, Pregnancy in Diabetics, Pregnancy, Animal, Prenatal Exposure Delayed Effects, Weight Gain, Rats, Sprague-Dawley, Insulin-Secreting Cells, Rats
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