Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 May;178(5):523-531.
doi: 10.1530/EJE-17-0882. Epub 2018 Mar 13.

Insulin-stimulated glucose uptake in skeletal muscle, adipose tissue and liver: a positron emission tomography study

Miikka-Juhani Honka  1 , Aino Latva-Rasku  1 , Marco Bucci  2 , Kirsi A Virtanen  1   3 , Jarna C Hannukainen  1 , Kari K Kalliokoski  1 , Pirjo Nuutila  4   5
Affiliations

Insulin-stimulated glucose uptake in skeletal muscle, adipose tissue and liver: a positron emission tomography study

Miikka-Juhani Honka et al. Eur J Endocrinol. 2018 May.

Abstract

Objective: Insulin resistance is reflected by the rates of reduced glucose uptake (GU) into the key insulin-sensitive tissues, skeletal muscle, liver and adipose tissue. It is unclear whether insulin resistance occurs simultaneously in all these tissues or whether insulin resistance is tissue specific.

Design and methods: We measured GU in skeletal muscle, adipose tissue and liver and endogenous glucose production (EGP), in a single session using 18F-fluorodeoxyglucose with positron emission tomography (PET) and euglycemic-hyperinsulinemic clamp. The study population consisted of 326 subjects without diabetes from the CMgene study cohort.

Results: Skeletal muscle GU less than 33 µmol/kg tissue/min and subcutaneous adipose tissue GU less than 11.5 µmol/kg tissue/min characterized insulin-resistant individuals. Men had considerably worse insulin suppression of EGP compared to women. By using principal component analysis (PCA), BMI inversely and skeletal muscle, adipose tissue and liver GU positively loaded on same principal component explaining one-third of the variation in these measures. The results were largely similar when liver GU was replaced by EGP in PCA. Liver GU and EGP were positively associated with aging.

Conclusions: We have provided threshold values, which can be used to identify tissue-specific insulin resistance. In addition, we found that insulin resistance measured by GU was only partially similar across all insulin-sensitive tissues studied, skeletal muscle, adipose tissue and liver and was affected by obesity, aging and gender.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Correlation of whole body glucose uptake (GU) with skeletal muscle GU (A), subcutaneous adipose tissue GU (B) and liver GU (C); correlation of skeletal muscle GU with subcutaneous adipose tissue GU (D) and liver GU (E); and correlation of subcutaneous adipose tissue GU with liver GU (F). GU values are from log10 transformed variables. Black regression line: men; gray regression line: women.
Figure 2
Figure 2
Correlation of endogenous glucose production with whole body glucose uptake (GU) (A), skeletal muscle GU (B), subcutaneous adipose tissue GU (C) and liver GU (D). GU values are from log10 transformed variables. Black regression line: men; gray regression line: women.
Figure 3
Figure 3
Whole body (M value), muscle, subcutaneous adipose tissue (SAT), intraperitoneal adipose tissue (VAT) and liver glucose uptake and endogenous glucose production (EGP) between insulin-sensitive (IS) and -resistant (IR) men and women. Dashed lines represent the optimal cutoff values between insulin-resistant and -sensitive individuals. The middle, bottom and top edges of the boxes represent median with 1st and 3rd quartiles, and notches are calculated as 1.58 × interquartile range/square root (n) (95% confidence interval for the median). If notches do not overlap, there is evidence for a difference between medians. The error bars extend to the furthest case inside 1.5 interquartile range from the box and outliers are presented as dots. ***P < 0.001, *P < 0.05.
See this image and copyright information in PMC

References

    1. DeFronzo RA. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes 2009. 58 773–795. (10.2337/db09-9028) - DOI - PMC - PubMed
    1. Iozzo P, Geisler F, Oikonen V, Mäki M, Takala T, Solin O, Ferrannini E, Knuuti J, Nuutila P. Insulin stimulates liver glucose uptake in humans: an 18F-FDG PET Study. Journal of Nuclear Medicine 2003. 44 682–689. - PubMed
    1. Virtanen KA, Lönnroth P, Parkkola R, Peltoniemi P, Asola M, Viljanen T, Tolvanen T, Knuuti J, Rönnemaa T, Huupponen R. et al Glucose uptake and perfusion in subcutaneous and visceral adipose tissue during insulin stimulation in nonobese and obese humans. Journal of Clinical Endocrinology and Metabolism 2002. 87 3902–3910. (10.1210/jcem.87.8.8761) - DOI - PubMed
    1. Utriainen T, Takala T, Luotolahti M, Rönnemaa T, Laine H, Ruotsalainen U, Haaparanta M, Nuutila P, Yki-Järvinen H. Insulin resistance characterizes glucose uptake in skeletal muscle but not in the heart in NIDDM. Diabetologia 1998. 41 555–559. (10.1007/s001250050946) - DOI - PubMed
    1. Virtanen KA, Iozzo P, Hällsten K, Huupponen R, Parkkola R, Janatuinen T, Lönnqvist F, Viljanen T, Rönnemaa T, Lönnroth P. et al Increased fat mass compensates for insulin resistance in abdominal obesity and type 2 diabetes: a positron-emitting tomography study. Diabetes 2005. 54 2720–2726. (10.2337/diabetes.54.9.2720) - DOI - PubMed

MeSH terms