Regulation of glucose homeostasis by glucocorticoids

Kuo, Taiyi; McQueen, Allison; Chen, Tzu-Chieh; Wang, Jen-Chywan

doi:10.1007/978-1-4939-2895-8_5

Cited by 723Estrogen and related hormone effectsPancreatic function and diabetesAdrenal Hormones and Disorders

Regulation of glucose homeostasis by glucocorticoids

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Kuo, Taiyi, McQueen, Allison, Chen, Tzu-Chieh, Wang, Jen-Chywan·2015·Advances in Experimental Medicine and Biology

DOI 10.1007/978-1-4939-2895-8_5PMC PMC6185996

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Abstract

Glucocorticoids are steroid hormones that regulate multiple aspects of glucose homeostasis. Glucocorticoids promote gluconeogenesis in liver, whereas in skeletal muscle and white adipose tissue they decrease glucose uptake and utilization by antagonizing insulin response. Therefore, excess glucocorticoid exposure causes hyperglycemia and insulin resistance. Glucocorticoids also regulate glycogen metabolism. In liver, glucocorticoids increase glycogen storage, whereas in skeletal muscle they play a permissive role for catecholamine-induced glycogenolysis and/or inhibit insulin-stimulated glycogen synthesis. Moreover, glucocorticoids modulate the function of pancreatic α and β cells to regulate the secretion of glucagon and insulin, two hormones that play a pivotal role in the regulation of blood glucose levels. Overall, the major glucocorticoid effect on glucose homeostasis is to preserve plasma glucose for brain during stress, as transiently raising blood glucose is important to promote maximal brain function. In this chapter we will discuss the current understanding of the mechanisms underlying different aspects of glucocorticoid-regulated mammalian glucose homeostasis.

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Over-exposure to GCs leads to hyperglycemia and insulin resistance.
“As a result, over-exposure to GCs leads to hyperglycemia and insulin resistance (22).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [22]
Long-term GCs therapy that oversteps beta-cell compensatory capacity begets impaired insulin secretion, hyperglycemia, and consequent type 2 diabetes.
“However, long-term GCs therapy that oversteps the beta-cell compensatory capacity begets impaired insulin secretion, hyperglycemia, and consequent type 2 diabetes (22).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [22]
Glucocorticoids facilitate gluconeogenesis in the liver and reduce glucose uptake and utilization by antagonizing insulin effects in white adipose tissue and skeletal muscle.
“Glucocorticoids facilitate the process of gluconeogenesis in the liver, while they reduce glucose uptake and utilization by antagonizing insulin effects in white adipose tissue and skeletal muscle.”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [22]
Excess GCs can cause compensatory beta-cell hyperplasia and hyperinsulinemia, with coexistence of normoglycemia.
“Research in murine models and human studies have shown excess GCs can cause compensatory beta-cell hyperplasia and hyperinsulinemia, with the coexistence of normoglycemia.”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [22]

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Background
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Authors: Kuo, T., McQueen, A., Chen, T.-C., & Wang, J.-C.
Affiliations: University of California, Berkeley (US)
Corresponding author: Wang, Jen-Chywan
ORCID: Kuo, Taiyi
Chen, Tzu-Chieh
Wang, Jen-Chywan
Venue: Advances in Experimental Medicine and Biology
Publisher: Springer New York
Published: 2015
Volume: 872
Pages: 99-126
ISSN: 0065-2598 (ISSN-L)
2214-8019
DOI: 10.1007/978-1-4939-2895-8_5
PMC: PMC6185996
OpenAlex: W1876389666
Cited by: 723
References: 193
Citations by year: 2026: 60 · 2025: 75 · 2024: 109 · 2023: 106 · 2022: 88 · 2021: 101 · 2020: 66 · 2019: 37 · 2018: 28 · 2017: 26 · 2016: 21 · 2015: 4
FWCI: 76.63
Type: book chapter
Language: en
Open access: green
europepmc.org
Locations: Advances in experimental medicine and biology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK83591, R01DK083591, T32DK061918)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords: glucocorticoids, glucose homeostasis, gluconeogenesis, insulin resistance, glycogen metabolism, glycogenolysis, glucagon secretion, insulin secretion, hyperglycemia, brain glucose supply, stress response, skeletal muscle, liver, white adipose tissue
MeSH terms: Animals, Glucocorticoids, Gluconeogenesis, Glucose, Glycogen, Homeostasis, Humans

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Regulation of glucose homeostasis by glucocorticoids

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