Relationship of insulin dynamics to body composition and resting energy expenditure following weight loss: Insulin, Body Composition, and Energy Expenditure
Open accessAbstract
OBJECTIVE: To examine associations of baseline insulin dynamics with changes in body composition and resting energy expenditure (REE) following weight loss. METHODS: Twenty-one participants with overweight or obesity achieved 10-15% weight loss and then received 3 weight loss maintenance diets (high-carbohydrate, moderate-carbohydrate, and low-carbohydrate) in random order, each for 4 weeks. Body composition was measured at baseline and after weight loss. Insulin 30 min after glucose consumption (insulin-30; insulin response), C-peptide deconvolution analysis, HOMA, hepatic insulin sensitivity (IS), and REE were assessed at baseline and after each maintenance diet. RESULTS: Insulin-30, but not maximal insulin secretion, hepatic IS, or HOMA, predicted changes in fat mass (standardized β = 0.385, 1.7 kg difference between 10th and 90th centile of insulin-30, P = 0.04) after weight loss. Insulin-30 (β = -0.341, -312 kcal day(-1) , P = 0.008), maximal insulin secretion (β = -0.216, -95 kcal day(-1) , P = 0.0002), HOMA (β = -0.394, -350 kcal day(-1) , P = 0.002), and hepatic IS (β = 0.217, 225 kcal day(-1) , P = 0.0003) predicted change in REE during weight loss maintenance, independent of changes in body composition. The inverse relationship between insulin-30 and REE was substantially attenuated when the low-carbohydrate diet was consumed first. CONCLUSIONS: These findings distinguish a novel phenotype, characterized by high insulin response, at risk for weight regain, and identify a dietary approach to ameliorate this risk.
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In humans, the relevance of this concept is supported by the observation that hyperinsulinemia following weight loss is predictive of weight regain.
“In humans, the relevance of this concept is supported by the observation that hyperinsulinemia following weight loss is predictive of weight regain [272].”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [272]
The Conclusion (page unavailable) says high insulin response measured before weight loss predicted adverse changes in body composition after weight loss and identified a phenotype at risk for weight regain. It does not report that hyperinsulinemia measured after weight loss predicted actual weight regain; the Abstract Results report changes in fat mass and resting energy expenditure instead. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIndividuals with high insulin secretion or other abnormalities of glucose homeostasis appear especially susceptible to adverse metabolic responses and weight gain when consuming a high-GL diet.
“Furthermore, studies suggest a unique diet–phenotype interaction, in that individuals with high insulin secretion or other abnormalities of glucose homeostasis appear especially susceptible to adverse metabolic responses and weight gain when consuming a high-GL diet (96, 105–110).”
From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [108]
Some trials have suggested that individuals with higher insulin secretion respond well to restricting carbohydrate intake for weight loss.
“Some trials have suggested that individuals with higher insulin secretion respond well to restricting carbohydrate intake for weight loss [50, 69].”
From Benefits of low carbohydrate diets: a settled question or still controversial? (2021) · cites this paper as [69]
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References 29 · Cited by 42
- Authors
- Hron, B. M., Ebbeling, C. B., Feldman, H. A., & Ludwig, D. S.
- Affiliations
- Boston Children's Hospital (US)
- Corresponding author
- Ludwig, David S.
- Venue
- Obesity
- Publisher
- Wiley
- Published
- 2015-09-16
- Volume
- 23
- Issue
- 11
- Pages
- 2216-2222
- ISSN
- 1930-7381 (ISSN-L)
- PMC
- PMC4633340
- OpenAlex
- W1841205805
- Cited by
- 42
- References
- 29
- Citations by year
- 2025: 4 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 5 · 2020: 4 · 2019: 2 · 2018: 10 · 2017: 5 · 2016: 3
- FWCI
- 5.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Obesity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Brigham and Women's Hospital
- Boston Children's Hospital
- Harvard Catalyst
- National Institutes of Health (UL1RR02575801)
- National Heart, Lung, and Blood Institute (F32HL122080)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK007477, K24DK082730, R01DK072428, T32DK007477, P30DK034854, P30DK040561)
- National Center for Research Resources (UL1RR025758, M01RR002635, M01RR002172)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Diet and metabolism studies
- Keywords
- insulin dynamics, insulin response, body composition, resting energy expenditure, weight loss, weight regain, overweight, low-carbohydrate diet, hepatic insulin sensitivity, fat mass, HOMA, insulin secretion
- MeSH terms
- Adult, Body Composition, Body Weight, C-Peptide, Diet, Reducing, Energy Metabolism, Female, Humans, Insulin, Insulin Resistance, Male, Obesity, Rest, Weight Loss, Overweight, Diet, Carbohydrate-Restricted, Young Adult
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