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Editorial
. 2020 Oct;27(5):1689-1697.
doi: 10.1007/s12350-018-01532-8. Epub 2018 Dec 13.

PET imaging of glucose and fatty acid metabolism for NAFLD patients

Affiliations
Editorial

PET imaging of glucose and fatty acid metabolism for NAFLD patients

Grant T Gullberg et al. J Nucl Cardiol. 2020 Oct.
No abstract available

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Conflict of interest statement

The other authors have no conflict of interest.

Figures

Figure 1.
Figure 1.
(A) Non-alcoholic fatty liver disease (NAFLD) is the excessive accumulation of fat in the liver of people who consume very little or no alcohol. Fat deposits (white/clear round/oval spaces) and mild fibrosis (green) are shown in a micrograph tissue sample of nonalcoholic fatty liver disease. The tissue is stained with Masson’s trichrome & Verhoeff stain. The hepatocytes stain red. Figure used under a Creative Commons Attribution-ShareAlike 3.0 Unported license (https://commons.wikimedia.org/wiki/File:Non-alcoholic_fatty_liver_disease1.jpg). (B) Liver has many functions in the body, including a major synthesize of very low density lipoproteins (VLDL) for cardiac lipoprotein-derived fatty acids. The ultra low-density lipoprotiens (ULDL) called chylomicrons are from dietary fat. Adipose triglyceride lipase may play an important role in developing NAFLD. This figure was originally in Science. 2011;332:1519, and reprinted with permission from AAAS. (C) Lipoprotein shown here as a micelle with a polar surface of phospholipid monolayer, free cholesterol, and apolipoproteins. The non-polar lipid core contains cholesterol esters, and triacylglycerides. Reprinted with permission from ShutterStock (ID: 246595399).
Figure 2.
Figure 2.
(A) Insulin binds to its receptor, which starts cascades of biochemical events including translocation of Glut-4 transporter to the plasma membrane and influx of glucose. Reprinted with permission from ShutterStock (ID:114645271) (B) Glycogen is the main storage of glucose in myocytes and is shown here in a two-dimensional cross-sectional contains a core protein of glycogen in surrounded by branches of glucose units (as many as 30,000). Public domain image (https://commons.wikimedia.org/wiki/File:Glycogen_structure.svg). (C) Electron transport chain of oxidative phosphorylation. The oxidation of NADH releases an electron which is transferred along the electron chain between protein complexes (Complex I, III, and IV) extruding H+ ions across the inner mitochondrial membrane into the space between the inner and outer mitochondrial membranes. The oxidation of FADH2 results in transferring of an electron between Complex II and III with the extrusion of H+ ions across the inner mitochondrial membrane. This produces ATP as H+ ions are transported back into the mitochondria by way of transport with ATP synthases converting ADP to ATP with the production of water. Reprinted from Nat Struct Mol Biol. 2017;24:800, by permission from Springer Nature.
Figure 3.
Figure 3.
(A) Insulin and contraction stimulates translocation of glucose and fatty acid cell membrane transporters. Reprinted from Prostaglandins, Leukotrienes and Essential Fatty Acids. 2010;82:149, with permission from Elsevier. (B) Carnitine shuttle transports fatty acids between cytoplasm and mitochondrion. The fatty acyl-CoA first combines with carnitine to form acyl-carnitine and eliminating CoA with the assist of CPT1. The fatty acyl-carnitine crosses the external mitochondrial membrane. Then the fatty acyl-carnitine crosses the internal mitochondrial membrane via CAT through facilitated diffusion. Carnitine is then exchanged for CoA by CPT2 to the original fatty acyl-CoA. The released carnitine diffuses back across the membrane by CAT into the mitochondrial intermembrane space. Reprinted with permission from ShutterStock (ID: 279851630). (C) Peroxisome proliferator-activated receptors (PPARs) regulate synthesis of enzymes for fatty acid metabolism by providing a high degree of transcriptional control of gene expression. Figure from https://upload.wikimedia.org/wikipedia/commons/4/43/PPAR-diagram.png, used under Creative Commons CC0 1.0 Universal Public Domain Dedication.

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References

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