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

Abstract

Type 2 diabetes mellitus (T2DM), one of the main types of Noncommunicable diseases (NCDs), is a systemic inflammatory disease characterized by dysfunctional pancreatic β-cells and/or peripheral insulin resistance, resulting in impaired glucose and lipid metabolism. Genetic, metabolic, multiple lifestyle, and sociodemographic factors are known as related to high T2DM risk. Dietary lipids and lipid metabolism are significant metabolic modulators in T2DM and T2DM-related complications. Besides, accumulated evidence suggests that altered gut microbiota which plays an important role in the metabolic health of the host contributes significantly to T2DM involving impaired or improved glucose and lipid metabolism. At this point, dietary lipids may affect host physiology and health via interaction with the gut microbiota. Besides, increasing evidence in the literature suggests that lipidomics as novel parameters detected with holistic analytical techniques have important roles in the pathogenesis and progression of T2DM, through various mechanisms of action including gut-brain axis modulation. A better understanding of the roles of some nutrients and lipidomics in T2DM through gut microbiota interactions will help develop new strategies for the prevention and treatment of T2DM. However, this issue has not yet been entirely discussed in the literature. The present review provides up-to-date knowledge on the roles of dietary lipids and lipidomics in gut-brain axis in T2DM and some nutritional strategies in T2DM considering lipids- lipidomics and gut microbiota interactions are given.

Keywords: Diet; Gut microbiota; Lipidomics; Lipids; 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) İmpaired glucose metabolisim. (11) İmpaired 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

Fig. 2

Interaction between impared glucose and lipids metabolism in T2DM. 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) İmpaired glucose metabolisim. (11) İmpaired 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 açil transferaz, G3P gliserol 3-fosfat protein kinase

Fig. 3

Gut-brain axis pathways related to T2DM. ENS enteric nervous system, SCFA short-chain fatty acid, LPS lipopolysaccharide

Fig. 4

Some nutritional strategies in T2DM considering lipidomics and gut microbiota interaction