The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Acute IL-6 treatment increases fatty acid turnover in elderly humans in vivo and in tissue culture in vitro
Abstract
To determine whether IL-6 increases lipolysis and fat oxidation in patients with type 2 diabetes and/or whether it exerts this effect independently of changes to the hormonal milieu, patients with type 2 diabetes (D) and healthy control subjects (CON) underwent recombinant human (rh)IL-6 infusion for 3 h. Rates of appearance (Ra) and disappearance (Rd) of [U-(13C)]palmitate and [6,6-(2H2)]glucose were determined. rhIL-6 infusion increased (P < 0.05) palmitate Ra and Rd in a similar fashion in both groups. Neither plasma glucose concentration nor glucose Ra/Rd was affected by rhIL-6 infusion in either group, whereas rhIL-6 infusion resulted in a reduction (P < 0.05) in circulating insulin in D. Plasma growth hormone (GH) was increased (P < 0.05) by IL-6 in CON, and cortisol increased (P < 0.05) in response to IL-6 in both groups. To determine whether IL-6 was exerting its effect directly or through activation of these hormones, we performed cell culture experiments. Fully differentiated 3T3-L1 adipocytes were treated with PBS (control) IL-6, or IL-6 plus dexamethasone and GH. IL-6 treatment alone increased (P < 0.05) lipolysis, but this effect was reduced by the addition of dexamethasone and GH such that IL-6 plus dexamethasone and GH had blunted (P < 0.05) lipolysis compared with IL-6 alone. To assess whether IL-6 increases fat oxidation, L6 myotubes were treated with PBS (Control), IL-6, or AICAR, a compound known to increase lipid oxidation. Both IL-6 and AICAR markedly increased (P < 0.05) oxidation of [(14)C]palmitate compared with Control. Acute IL-6 treatment increased fatty acid turnover in D patients as well as healthy CON subjects. Moreover, IL-6 appears to be activating lipolysis independently of elevations in GH and/or cortisol and appears to be a potent catalyst for fat oxidation in muscle cells.
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In the citing paper
“Together, these coordinated actions of IL-6 enhance metabolic flexibility by simultaneously facilitating glucose uptake and endogenous glucose production, a process thought to be a consequence of the permissive effect of IL-6 on glucagon and cortisol secretion [51].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [51]
In the citing paper
“However, in human subjects, an in vivo IL-6 infusion does not alter splanchnic glucose output (30,31).”
From Signaling Specificity of Interleukin-6 Action on Glucose and Lipid Metabolism in Skeletal Muscle (2006) · cites this paper as [30]
In the citing paper
“When diabetes patients were given an rhIL-6 infusion, plasma concentrations of insulin decreased to levels comparable with that in age and BMI (body mass index)-matched healthy controls, indicating that the IL-6 enhanced insulin sensitivity [50].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [50]
In the citing paper
“A number of studies indicate that IL-6 enhances lipolysis, as well as fat oxidation [50, 58].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [50]
In the citing paper
“Infusion of rhIL-6 into healthy humans to obtain physiological concentrations of IL-6 increased lipolysis in the absence of hypertriacylglyceridemia or changes in catecholamines, glucagon, insulin, or any adverse effects in healthy individuals as well as patients with type 2 diabetes [49, 50, 58].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [50]
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Self-citation
Metadata
- Authors
- Petersen, E. W., Carey, A. L., Sacchetti, M., Steinberg, G. R., Macaulay, S. L., Febbraio, M. A., & Pedersen, B. K.
- Affiliations
- University of Copenhagen (DK)
- RMIT University (AU)
- The University of Melbourne (AU)
- Commonwealth Scientific and Industrial Research Organisation (AU)
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2005-01
- Volume
- 288
- Issue
- 1
- Pages
- E155-E162
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2145229644
- Cited by
- 311
- References
- 33
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 18 · 2023: 10 · 2022: 16 · 2021: 17 · 2020: 11 · 2019: 11 · 2018: 14 · 2017: 14 · 2016: 9 · 2015: 9 · 2014: 17 · 2013: 26 · 2012: 22
- FWCI
- 9.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- interleukin-6, lipolysis, fat oxidation, fatty acid turnover, type 2 diabetes, adipocytes, skeletal muscle, growth hormone, cortisol, dexamethasone, insulin, AICAR, palmitate, 3T3-L1 adipocytes, L6 myotubes, older adults
- MeSH terms
- Aged, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Glycerol, Hormones, Humans, Insulin, Lipolysis, Male, Middle Aged, Triglycerides, Interleukin-6, 3T3-L1 Cells, Mice, In Vitro Techniques
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