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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: The roles of dietary lipids and lipidomics in gut-brain axis in type 2 diabetes mellitus

Fig. 1

The active role of insulin in normoglycemia and normolipidemia. An overview of Interaction between impared glucose and lipids metabolisim inT2DM. (1) increased chylomicron production, (2) reduced catabolism of both chylomicrons and VLDLs (diminished LPL activity), (3)increased VLDL production (mostly VLDL1), (4) reduced LDL turnover (5) increased production of large VLDL (VLDL1) preferentially taken up by macrophages; LDL (qualitative and kinetic abnormalities): (6) low plasma adiponectin favouring the increase in HDL catabolism. (7) increased number of glycated LDLs, small, dense LDLs (TAG-rich) and oxidised LDLs, which are preferentially taken up by macrophages; (8) increased CETP activity (increased transfer of triacylglycerols from TAG-rich lipoproteins to LDLs and HDLs), (9) increased TAG content of HDLs, promoting HL activity and HDL catabolism, (10) Ä°mpaired glucose metabolisim. (11) Ä°mpaired de novo lipid metabolisim (Acetyl CoA and NADPH inhibit pyruvate dehydrogenase as a result of B oxidation. The lactate and alalnin thus formed increase hyperglycemia because of gluconeogenesis (ketone bodies formation increases) in the liver.) CE cholesterol ester, CETP cholesteryl ester transfer protein, HDLn nascent HDL, HL hepatic lipase, HSL hormone-sensitive lipase, LPL lipoprotein lipase, SR-B1 scavenger receptor B1, TAG triacylglycerol, PP protein phosphatase, PK protein kinase, NEFA non-esterified fatty acids DNL: de novo lipogenesis, LCAT Lesitin-kolesterol acil transferaz, G3P gliserol 3-fosfat protein kinase

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