Adipose tissue as a buffer for daily lipid flux

Frayn, K.

doi:10.1007/s00125-002-0873-y

Cited by 752Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismLipid metabolism and biosynthesis

Adipose tissue as a buffer for daily lipid flux

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Frayn, K.·2002·Diabetologia

DOI 10.1007/s00125-002-0873-y

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Abstract

Insulin resistance occurs in obesity and Type II (non-insulin-dependent) diabetes mellitus, but it is also a prominent feature of lipodystrophy. Adipose tissue could play a crucial part in buffering the flux of fatty acids in the circulation in the postprandial period, analogous to the roles of the liver and skeletal muscle in buffering postprandial glucose fluxes. Adipose tissue provides its buffering action by suppressing the release of non-esterified fatty acids into the circulation and by increasing triacylglycerol clearance. In particular, the pathway of 'fatty acid trapping' (adipocyte uptake of fatty acids liberated from plasma triacylglycerol by lipoprotein lipase) could play a key part in the buffering process. If this buffering action is impaired, then extra-adipose tissues are exposed to excessive fluxes of lipid fuels and could accumulate these in the form of triacylglycerol, leading to insulin resistance. These tissues will include liver, skeletal muscle and the pancreatic beta cell, where the long term effect is to impair insulin secretion. Adipose tissue buffering of lipid fluxes is impaired in obesity through defects in the ability of adipose tissue to respond rapidly to the dynamic situation that occurs after meals. It is also impaired in lipodystrophy because there is not sufficient adipose tissue to provide the necessary buffering capacity. Thus, the phenotype, at least with regard to insulin resistance, is similar with both excess and deficiency of adipose tissue. Furthermore, this concept could provide a framework for understanding the action of the thiazolidinedione insulin-sensitizing agents.

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Fatty acids derived from a meal trigger adipose tissue to reduce nonesterified fatty acid release and prompt hepatocytes to reduce endogenous triacylglycerol release, together stimulating clearance of circulating triacylglycerol.
“Fatty acids derived from a meal trigger adipose tissue to reduce nonesterified fatty acid release and prompt hepatocytes to reduce endogenous triacylglycerol release, together stimulating the clearance of circulating triacylglycerol (19).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [19]
The capacity to store and release FFA from adipose tissue may influence metabolic flexibility.
“Since adipose tissue is the main source of plasma FFA, the capacity to store and release FFA from adipose tissue may influence metabolic flexibility ([11](#r11)).”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [11]

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Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse
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Authors: Frayn, K.
Affiliations: University of Oxford (GB)
Corresponding author: Frayn, K.
ORCID: Frayn, K.
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 2002-07-24
Volume: 45
Issue: 9
Pages: 1201-1210
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s00125-002-0873-y
OpenAlex: W2054800029
Cited by: 752
References: 127
Citations by year: 2026: 14 · 2025: 19 · 2024: 20 · 2023: 29 · 2022: 33 · 2021: 38 · 2020: 37 · 2019: 38 · 2018: 42 · 2017: 40 · 2016: 29 · 2015: 38 · 2014: 35 · 2013: 38 · 2012: 34
FWCI: 3.53
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Diabetologia (publishedVersion)
PubMed (publishedVersion)
Funders: Novo Nordisk
Topics: Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords: adipose tissue, insulin resistance, obesity, type 2 diabetes, lipodystrophy, free fatty acids, lipoprotein lipase, hepatic lipid metabolism, skeletal muscle lipid metabolism, pancreatic beta-cell insulin secretion, thiazolidinediones, insulin sensitizers
MeSH terms: Adipose Tissue, Animals, Fatty Acids, Glucose, Humans, Insulin Resistance, Lipodystrophy, Lipoprotein Lipase, Liver, Triglycerides, Muscle, Skeletal, Postprandial Period, Lipid Metabolism

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Adipose tissue as a buffer for daily lipid flux

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