CD36 Modulates Fasting and Preabsorptive Hormone and Bile Acid Levels

Bile acids are involved in the emulsification and absorption of dietary fats, as well as acting as signaling molecules. Recently, bile acid signaling through farnesoid X receptor and G protein-coupled bile acid receptor (TGR5) has been reported to elicit changes in not only bile acid synthesis but also metabolic processes, including the alteration of gluconeogenic gene expression and energy expenditure. A role for bile acids in glucose metabolism is also supported by a correlation between changes in the metabolic state of patients (i.e., obesity or postbariatric surgery) and altered serum bile acid levels. However, despite evidence for a role for bile acids during metabolically challenging settings, the direct effect of elevated bile acids on insulin action in the absence of metabolic disease has yet to be investigated. The present study examines the impact of acutely elevated plasma bile acid levels on insulin sensitivity using hyperinsulinemic-euglycemic clamps. In wild-type mice, elevated bile acids impair hepatic insulin sensitivity by blunting the insulin suppression of hepatic glucose production. The impaired hepatic insulin sensitivity could not be attributed to TGR5 signaling, as TGR5 knockout mice exhibited a similar inhibition of insulin suppression of hepatic glucose production. Canonical insulin signaling pathways, such as hepatic PKB (or Akt) activation, were not perturbed in these animals. Interestingly, bile acid infusion directly into the portal vein did not result in an impairment in hepatic insulin sensitivity. Overall, the data indicate that acute increases in circulating bile acids in lean mice impair hepatic insulin sensitivity via an indirect mechanism.

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“…Bile acid measurements. Bile acids were measured by liquid chromatography-mass spectrometry, as previously described (3,21,52).…”

Section: Methodsmentioning

confidence: 99%

Systemic bile acids induce insulin resistance in a TGR5-independent manner

Syring

Cyphert

Beck

et al. 2019

American Journal of Physiology-Endocrinology and Metabolism

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“…Genetic variants in CD36 have been associated with modulation of lipid metabolism, coronary artery disease (CAD), IR, familial T2DM, and increased body mass index (BMI) (10,13). Genomewide association (GWA) studies revealed that 15 CD36 single-nucleotide variants (SNVs) have been associated with risk of stroke, obesity, and left ventricular mass (2,14). The SNV rs3211938 in CD36 (also known as T1264G and T188G) is a coding variant identified in exon X at the 188 nucleotide that inserts a stop codon at amino acid 325, resulting in a truncated protein associated with a reduction of CD36 levels by around 50 % (15).…”

Section: Introductionmentioning

confidence: 99%

Contribution of rs3211938 polymorphism at CD36 to glucose levels, oxidized low-density lipoproteins, insulin resistance, and body mass index in Mexican mestizos with type-2 diabetes from western Mexico

Martín-Márquez¹,

Sandoval-García²,

Mercado³

et al. 2021

Nutr Hosp

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Contribución del polimorfismo rs3211938 de CD36 a los niveles de glucosa, las lipoproteínas de baja densidad oxidadas, la resistencia a la insulina y el índice de masa corporal en mestizos mexicanos con diabetes de tipo 2 del occidente de México Contribution of rs3211938 polymorphism at CD36 to glucose levels, oxidized low-density lipoproteins, insulin resistance, and body mass index in Mexican mestizos with type-2 diabetes from western Mexico 10.20960/nh.03447 OR 3447 Contribution of rs3211938 polymorphism at CD36 to glucose levels, oxidized low-density lipoproteins, insulin resistance, and body mass index in Mexican mestizos with type-2 diabetes from western Mexico Contribución del polimorfismo rs3211938 de CD36 a los niveles de glucosa, las lipoproteínas de baja densidad oxidadas, la resistencia a la insulina y el índice de masa corporal en mestizos mexicanos con diabetes de tipo 2 del occidente de México

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“…CD36 has also been reported to interact with incretins, including GLPs and GIP. The secretion of GLP-1 and GIP to a high-fat meal was significantly reduced in human subjects carrying CD36 rs3211938 (G/T) which decreases CD36 level by approximately 50% ( Shibao et al, 2018 ). In the meantime, the secretion of ghrelin, a gastric peptide regulating growth and energy balance, was unchanged in rs3211938 subjects ( Shibao et al, 2018 ), suggesting that CD36 may not regulates the secretion of ghrelin.…”

Section: Introductionmentioning

confidence: 99%

CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine

Zhao

Ding

et al. 2021

Front. Physiol.

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Dietary lipids absorbed in the intestine are closely related to the development of metabolic syndrome. CD36 is a multi-functional scavenger receptor with multiple ligands, which plays important roles in developing hyperlipidemia, insulin resistance, and metabolic syndrome. In the intestine, CD36 is abundant on the brush border membrane of the enterocytes mainly localized in proximal intestine. This review recapitulates the update and current advances on the importance of intestinal CD36 in sensing dietary lipids and regulating intestinal lipids uptake, synthesis and transport, and regulating intestinal hormones secretion. However, further studies are still needed to demonstrate the complex interactions between intestinal CD36 and dietary lipids, as well as its importance in diet associated metabolic syndrome.

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CD36 Modulates Fasting and Preabsorptive Hormone and Bile Acid Levels

Abstract: CD36 plays an important role in the preabsorptive hormone and BA responses that coordinate brain and gut regulation of energy metabolism.

Cited by 9 publications

References 56 publications

Systemic bile acids induce insulin resistance in a TGR5-independent manner

Systemic bile acids induce insulin resistance in a TGR5-independent manner

Contribution of rs3211938 polymorphism at CD36 to glucose levels, oxidized low-density lipoproteins, insulin resistance, and body mass index in Mexican mestizos with type-2 diabetes from western Mexico

CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine

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