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Cited by 155Diabetes Management and ResearchDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes Treatment and Management

Intensive insulin therapy and weight gain in IDDM

Carlson, Michael G, Campbell, Peter J·1993·Diabetes
DOI 10.2337/diab.42.12.1700
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Abstract

Intensive insulin therapy is frequently complicated by excessive weight gain. The purpose of this study was to determine the cause and composition of this weight gain. Therefore, changes in body composition, energy expenditure, glycosuria, and substrate kinetics were evaluated in patients with IDDM who transferred from conventional insulin therapy to intensive insulin therapy. Six adult patients with IDDM were studied on conventional insulin therapy and after 2 mo of intensive insulin therapy while maintaining constant caloric intake and were compared with a group of 6 matched nondiabetic volunteers. Body composition was determined by underwater weighing. Energy expenditure was measured during 24-h stays in a whole-room calorimeter. Whole-body turnover rates of glucose, glycerol, palmitate, and leucine were determined by isotope dilution methods. Intensive insulin therapy lowered the mean daily blood glucose concentration and HbA1 (14.8 ± 1.6 to 7.7 ± 0.6 mM and 12.9 ± 0.9 to 9.6 ± 0.6%, both P < 0.01) and almost eliminated glycosuria (428 ± 116 to 39 ± 22 mmol/day, P < 0.05). Body weight increased 2.6 ± 0.8 kg with intensive insulin therapy (P < 0.05) as a result of an increase in fat mass (2.4 ± 0.8 kg, P < 0.05). Daily energy expenditure decreased 5% (118 ± 32 kcal/day) with intensive insulin therapy (P < 0.05). The rates of glucose, glycerol, free fatty acid, and leucine turnover, triglyceride/free fatty acid cycling, and nonoxidative glucose and protein disposal were reduced in the diabetic volunteers during intensive insulin therapy. Thus, intensive insulin therapy causes an increase in body fat as a result of the elimination of glycosuria and reduction in 24-h energy expenditure. The elimination of glycosuria contributed 70% to the positive energy balance during intensive insulin therapy, and the reduction in 24-h energy expenditure contributed the remainder. The reduction in 24-h energy expenditure was the result of the decrease in triglyceride/free fatty acid cycling and nonoxidative glucose and protein metabolism.

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  • Possible reasons for smaller weight reductions in diabetes include lower resting metabolic rate after better glycemic control, poorer dietary adherence and defensive snacking from hypoglycemia fear, and less glycosuria.

    “Mechanisms responsible for smaller weight losses in patients with diabetes may include reductions in resting metabolic rate, which occur with improved glycemic control (accompanying weight loss), decreased dietary adherence and “defensive snacking” related to fears of hypoglycemia, as well as reduced glycosuria.(49, 50)”

    From Semaglutide for the treatment of obesity (2023) · cites this paper as [49]

  • Patients with type 1 diabetes undergoing intensification of insulin therapy for 2 mo experienced a 2.4-kg increase in body fat, associated with decreased energy expenditure and therefore not fully attributable to changes in dietary intake and urinary glucose excretion.

    “Patients with type 1 diabetes undergoing intensification of insulin therapy for 2 mo experienced a 2.4-kg increase in body fat, associated with decreased energy expenditure and therefore not fully attributable to changes in dietary intake and urinary glucose excretion (70).”

    From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [70]

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Authors
Carlson, M. G., & Campbell, P. J.
Affiliations
Vanderbilt University (US)
ORCID
Campbell, Peter J
Venue
Diabetes
Publisher
American Diabetes Association
Published
1993-12-01
Volume
42
Issue
12
Pages
1700-1707
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.42.12.1700
OpenAlex
W2119063869
Cited by
155
References
0
Citations by year
2026: 2 · 2025: 3 · 2024: 5 · 2023: 3 · 2022: 9 · 2021: 9 · 2020: 4 · 2018: 4 · 2017: 6 · 2016: 6 · 2015: 2 · 2014: 4 · 2013: 9 · 2012: 3
FWCI
2.61
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r29dk041376-05)
  • U.S. Public Health Service (P30-26657, P60 20593)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK41376)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
intensive insulin therapy, type 1 diabetes, weight gain, body composition, fat mass, energy expenditure, glycosuria, substrate kinetics, glucose turnover, nonoxidative glucose disposal, protein metabolism, HbA1c
MeSH terms
Adipose Tissue, Adult, Basal Metabolism, Blood Glucose, Diabetes Mellitus, Type 1, Fatty Acids, Nonesterified, Female, Glycerol, Humans, Insulin, Male, Weight Gain, Body Mass Index

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