Effects of fasting on insulin action and glucose kinetics in lean and obese men and women
Abstract
The development of insulin resistance in the obese individual could impair the ability to appropriately adjust metabolism to perturbations in energy balance. We investigated a 12- vs. 48-h fast on hepatic glucose production (R a ), peripheral glucose uptake (R d ), and skeletal muscle insulin signaling in lean and obese subjects. Healthy lean [ n = 14; age = 28.0 ± 1.4 yr; body mass index (BMI) = 22.8 ± 0.42] and nondiabetic obese ( n = 11; age = 34.6 ± 2.3 yr; BMI = 36.1 ± 1.5) subjects were studied following a 12- and 48-h fast during 2 h of rest and a 3-h 40 mU·m −2 ·min −1 hyperinsulinemic-euglycemic clamp (HEC). Basal glucose R a decreased significantly from the 12- to 48-h fast (lean 1.96 ± 0.23 to 1.63 ± 0.15; obese 1.23 ± 0.07 to 1.07 ± 0.07 mg·kg −1 ·min −1 ; P = 0.004) and was equally suppressed during the HEC after both fasts. The increase in glucose R d during the HEC after the 12-h fast was significantly decreased in lean and obese subjects after the 48-h fast (lean 9.03 ± 1.17 to 4.16 ± 0.34, obese 6.10 ± 0.77 to 3.56 ± 0.30 mg·kg FFM −1 ·min −1 ; P < 0.001). After the 12- but not the 48-h fast, insulin-stimulated AKT Ser 473 phosphorylation was greater in lean than obese subjects. We conclude that 1) 48 h of fasting produces a marked decline in peripheral insulin action, while suppression of hepatic glucose production is maintained in lean and obese men and women; and 2) the magnitude of this decline is greater in lean vs. obese subjects.
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The reduction in insulin-stimulated glucose uptake observed in the present study confirms previous observations showing that prolonged fasting reduced glucose Rd, which was accounted for by a reduction in both insulin-stimulated glucose oxidation and nonoxidative glucose disposal.
“The reduction in insulin-stimulated glucose uptake observed in the present study confirms previous observations showing that prolonged fasting reduced glucose Rd, which was accounted for by a reduction in both insulin-stimulated glucose oxidation and nonoxidative glucose disposal (40).”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [40]
Prolonged fasting reduced glucose Rd, which was accounted for by a reduction in both insulin-stimulated glucose oxidation and nonoxidative glucose disposal.
“previous observations showing that prolonged fasting reduced glucose Rd, which was accounted for by a reduction in both insulin-stimulated glucose oxidation and nonoxidative glucose disposal (40).”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [40]
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- Authors
- Bergman, B. C., Cornier, M.-A., Horton, T. J., & Bessesen, D. H.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2007-10
- Volume
- 293
- Issue
- 4
- Pages
- E1103-E1111
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2155793170
- Cited by
- 87
- References
- 52
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 8 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 5
- FWCI
- 5.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K24DK002935, F32DK059739, DK-02935, DK-059739)
- National Center for Research Resources (K23RR016185, RR.00036)
- Topics
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- fasting, insulin resistance, obesity, hepatic glucose production, peripheral glucose uptake, skeletal muscle insulin signaling, Akt Ser473 phosphorylation, hyperinsulinemic-euglycemic clamp, energy balance
- MeSH terms
- Adult, Basal Metabolism, Blood Glucose, Fasting, Fatty Acids, Nonesterified, Female, Humans, Insulin, Male, Obesity, Pulmonary Gas Exchange, Receptor, Insulin, Thinness, Glucose Clamp Technique, Muscle, Skeletal
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