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Cited by 497Diabetes Management and ResearchAdipokines, Inflammation, and Metabolic DiseasesAdvanced Glycation End Products research

Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises

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Stentz, Frankie B., Umpierrez, Guillermo E., Cuervo, Ruben, Kitabchi, Abbas E.·2004·Diabetes
DOI 10.2337/diabetes.53.8.2079
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Abstract

Acute and chronic hyperglycemia are proinflammatory states, but the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks is not known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH). We studied 20 lean and 28 obese patients with DKA, 10 patients with NKH, and 12 lean and 12 obese nondiabetic control subjects. We measured 1) proinflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-6, IL1-β, and IL-8), 2) markers of cardiovascular risk (C-reactive protein [CRP], homocysteine, and plasminogen activator inhibitor-1 [PAI-1]), 3) products of reactive oxygen species (ROS; thiobarbituric acid [TBA]-reacting material, and dichlorofluorescein [DCF]), and 4) cortisol, growth hormone (GH), and free fatty acids (FFAs) on admission (before insulin therapy) and after insulin therapy and resolution of hyperglycemia and/or ketoacidosis. Results were compared with lean and obese control subjects. Circulating levels of cytokines, TBA, DCF, PAI-1, FFAs, cortisol, and GH on admission were significantly increased two- to fourfold in patients with hyperglycemic crises compared with control subjects, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises. Changes in CRP and homocysteine in response to insulin therapy did not reach control levels after resolution of hyperglycemia. We conclude that DKA and NKH are associated with elevation of proinflammatory cytokines, ROS, and cardiovascular risk factors in the absence of obvious infection or cardiovascular pathology. Return of these values to normal levels with insulin therapy demonstrates a robust anti-inflammatory effect of insulin.

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  • Severe insulin deficiency can cause acute hyperglycemic complications such as diabetic ketoacidosis, hyperosmolar hyperglycemic state, hypertriglyceridemia, and hypercatabolic state, which may be life-threatening.

    “Absolute (or near-absolute) insulin deficiency can result in acute hyperglycemic complications, including DKA, hyperosmolar hyperglycemic state, hypertriglyceridemia, and hypercatabolic state, which can be life-threatening.1114–1120”

    From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [1114]

    The introduction (page unavailable) describes DKA and nonketotic hyperglycemia as acute hyperglycemic emergencies characterized by decreased effective insulin and severe alterations in protein, lipid, and carbohydrate metabolism. The copy does not identify nonketotic hyperglycemia as hyperosmolar hyperglycemic state or describe hypertriglyceridemia and a hypercatabolic state as separate complications. The Discussion (page unavailable) associates hyperglycemia in critical-care patients with increased mortality, but does not establish that every listed complication can be life-threatening. (LLM, conf=0.86)

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  • Most studies identifying roles of adipose hormones were performed in rodents, and their immune and insulin-sensitising effects in humans remain unclear.

    “It should be noted that most studies identifying the roles of these hormones have been performed in rodents and the immune and insulin-sensitising effects of these hormones in humans remain unclear (20,21) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [20]

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Authors
Stentz, F. B., Umpierrez, G. E., Cuervo, R., & Kitabchi, A. E.
Affiliations
University of Tennessee Health Science Center (US)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2004-08-01
Volume
53
Issue
8
Pages
2079-2086
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.53.8.2079
OpenAlex
W2170652400
Cited by
497
References
62
Citations by year
2026: 10 · 2025: 20 · 2024: 28 · 2023: 34 · 2022: 45 · 2021: 23 · 2020: 35 · 2019: 15 · 2018: 22 · 2017: 16 · 2016: 25 · 2015: 22 · 2014: 24 · 2013: 15 · 2012: 25
FWCI
12.61
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • Deutsches Krebsforschungszentrum
  • National Institutes of Health
  • National Center for Research Resources (RR 00211, M01RR000211)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Keywords
diabetic ketoacidosis, nonketotic hyperglycemia, hyperglycemic crisis, inflammatory cytokines, oxidative stress, lipid peroxidation, cardiovascular risk markers, C-reactive protein, homocysteine, plasminogen activator inhibitor-1, TNF-α, interleukin-6, IL-1β, interleukin-8, insulin therapy, free fatty acids, cortisol, growth hormone, obesity
MeSH terms
Adult, C-Reactive Protein, Diabetes Mellitus, Diabetic Angiopathies, Fatty Acids, Nonesterified, Female, Homocysteine, Humans, Hydrogen-Ion Concentration, Hyperglycemia, Male, Middle Aged, Obesity, Reference Values, Lipid Peroxidation, Biomarkers, Body Mass Index, Cytokines, Diabetic Ketoacidosis, Plasminogen Activator Inhibitor 1, Oxidative Stress

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