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Cited by 319Lipid metabolism and disordersDiabetes, Cardiovascular Risks, and LipoproteinsLipid metabolism and biosynthesis

Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM.

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Malmström, R., Packard, C. J., Caslake, M., Bedford, D., Stewart, P., Yki-Järvinen, H., Shepherd, J., Taskinen, M.-R.·1997·Diabetologia
DOI 10.1007/s001250050700
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Abstract

Insulin administration to healthy subjects inhibits the production of very low density lipoprotein (VLDL)1 (Svedbergs flotation (Sf) rate 60-400) without affecting that of VLDL2 (Sf 20-60) sub-class. This study was designed to test whether this hormonal action is impaired in non-insulin-dependent diabetes mellitus (NIDDM). We studied six men with NIDDM (age 53 +/- 3 years, body mass index 27.0 +/- 1.0 kg/m2, plasma triglycerides 1.89 +/- 0.22 mmol/l) during an 8.5 h infusion of saline (control) and then in hyperinsulinaemic (serum insulin approximately 540 pmol/l) conditions during 8.5 h infusions of glucose and insulin to give either hyper- and normoglycaemic conditions. [3-2H]-leucine was used as tracer and kinetic constants derived using a non-steady-state multicompartmental model. Compared to the control study, patients with NIDDM reduced VLDL1 apo B production by only 3 +/- 8% after 8.5 h of hyperinsulinaemia (701 +/- 102 vs 672 +/- 94 mg/day respectively, NS) in hyperglycaemic conditions and by 9 +/- 21% under normoglycaemic conditions (603 +/- 145 mg/day). In contrast, in normal subjects insulin induced a 50 +/- 15% decrement in VLDL1 apo B production (p < 0.05). Direct synthesis of VLDL2 apo B in patients with NIDDM was not markedly affected by insulin. We conclude that a contributory factor to hypertriglyceridaemia in NIDDM is the inability of insulin to inhibit acutely the release of VLDL1 from the liver, despite efficient suppression of serum nonesterfied fatty acids.

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  • Hepatic insulin resistance may contribute to a high production rate of VLDL because insulin reduces apoB synthesis and VLDL secretion in the liver.

    “Hepatic insulin resistance may contribute to a high production rate of VLDL because insulin reduces apoB synthesis and VLDL secretion in the liver (66, 67).”

    From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [66]

    The Results and Discussion report that insulin suppresses VLDL1 apo B production and release in healthy subjects, but that this response is impaired in patients with NIDDM. The paper specifies that VLDL2 secretion is unchanged and does not establish a general reduction in apoB synthesis or secretion of all VLDL. (LLM, conf=0.86)

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Research works printed but not linked: 3

  1. Malmstro ¨m R, Packard CJ, Watson TDG et al. (1997) Met- abolic basis of hypotriglyceridemic effects of insulin in nor- mal men. Arterioscler Thromb Vasc Biol. (In press)
  2. Lindgren FT, Jensen LC (1972) The isolation and quantita- tive analysis of serum lipoproteins. In: Nelson GJ (ed) Blood lipids and lipoproteins: Quantitation, composition and metabolism. John Wiley & Sons, Livermore, Califor- nia, pp 182-217
  3. Hardman DA, Kane JP (1986) Isolation and characterisa- tion of apolipoprotein B-48. In: Segrest JP, Albers JJ (eds) Methods in enzymology. Plasma lipoproteins (Part A): Preparation, structure and molecular biology, 128. Aca- demic Press, Orlando, pp 247-262

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Authors
Malmström, R., Packard, C. J., Caslake, M., Bedford, D., Stewart, P., Yki-Järvinen, H., Shepherd, J., & Taskinen, M.-R.
Affiliations
  • University of Helsinki (FI)
  • Glasgow Royal Infirmary (GB)
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
1997-03-20
Volume
40
Issue
4
Pages
454-462
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s001250050700
OpenAlex
W2167130513
Cited by
319
References
39
Citations by year
2026: 2 · 2025: 1 · 2024: 3 · 2023: 7 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 4 · 2016: 12 · 2015: 12 · 2014: 15 · 2013: 15 · 2012: 12
FWCI
9.25
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
Funders
British Heart Foundation
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
type 2 diabetes, insulin resistance, triglyceride metabolism, VLDL, VLDL1, apolipoprotein B, hepatic lipoprotein secretion, hypertriglyceridemia, hyperinsulinemia, hyperglycemia, free fatty acids
MeSH terms
Apolipoproteins B, Cholesterol, Deuterium, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Humans, Hyperglycemia, Hyperinsulinism, Infusions, Intravenous, Insulin, Leucine, Cholesterol, HDL, Lipoproteins, VLDL, Liver, Male, Middle Aged, Models, Biological, Radioisotope Dilution Technique, Reference Values, Triglycerides, Glucose Clamp Technique

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