CD36 regulates fatty acid composition and sensitivity to insulin in 3T3-L1 adipocytes

Kontrová, K.; Zídková, J.; Bartos, B.; Škop, Vojtěch; Sajdok, J.; Kazdová, Ludmila; Mikulík, K.; Mlejnek, Petr; Zidek, Vaclav; Pravenec, Michal

doi:10.33549/physiolres.931324

Cited by 18 publications

(2 citation statements)

References 20 publications

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“…CD36 is an important factor in fatty acid uptake. Increased expression of CD36 in the adipose tissue has been linked to insulin resistance in in vitro (45) and humans (46,47).…”

Section: Discussionmentioning

confidence: 99%

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Human Soluble Prorenin Receptor Expressed in Adipose Tissue Improves Insulin Sensitivity and Endothelial Function in Obese Female Mice

Arthur,

Ahmed,

Nichols

et al. 2024

Preprint

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Increased circulating levels of the soluble prorenin receptor (sPRR), a component of the renin angiotensin system (RAS), plays a role in obesity, glucose, and insulin homeostasis. However, elevated plasma sPRR in diabetic patients has been shown correlated with hyperglycemia in women but not men. Hence, the current study sought to understand the contribution of human sPRR (HsPRR) produced in the adipose tissue (Adi) on adipogenesis, and glucose and insulin balance in obesity settings. Adi-HsPRR mice were generated by breeding human sPRR-Myc-tag transgenic mice with mice expressing Adiponectin/Cre. The mouse model was validated by detecting 28kDa myc-tagged HsPRR by western blotting. Adipose HsPRR expression did not change circulating sPRR in female mice fed a standard chow diet or high fat diet (HFD) but increased plasma sPRR in male Adi-HsPRR mice fed a HFD compared to HFD-fed controls. Yet, Adi-HsPRR improved insulin sensitivity, vascular relaxation and the vasodilator agent Ang 1-7 in obese female mice but not in the male counterparts. Moreover, Adi-HsPRR expression reduced the expression of the adipogenic genes SREBP1C and CD36 only in gonadal white adipose from obese female mice, signifying that adipose tissue-derived HsPRR exerts a sex-specific effect on insulin sensitivity and endothelial function which seems independent of circulating sPRR.

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“…CD36 is an important factor in fatty acid uptake. Increased expression of CD36 in the adipose tissue has been linked to insulin resistance in in vitro (45) and humans (46,47).…”

Section: Discussionmentioning

confidence: 99%

“…CD36 is an important factor in fatty acid uptake. Increased expression of CD36 in the adipose tissue has been linked to insulin resistance in in vitro ( 45 ) and humans (46, 47). Likewise, Adi-HsPRR in females decreased CD36 expression in gonadal WAT which is linked to the improved insulin response observed.…”

Section: Discussionmentioning

confidence: 99%

Human Soluble Prorenin Receptor Expressed in Adipose Tissue Improves Insulin Sensitivity and Endothelial Function in Obese Female Mice

Arthur,

Ahmed,

Nichols

et al. 2024

Preprint

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Adipose Carbonylation and Mitochondrial Dysfunction

Hauck

Olson

Burrill

et al. 2017

Protein Carbonylation

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Gamma-Linolenic Acid Suppresses NF-κΒ Signaling via CD36 in the Lipopolysaccharide-Induced Inflammatory Response in Primary Goat Mammary Gland Epithelial Cells

et al. 2016

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Gamma-linolenic acid (GLA) and linoleic acid (LA), which are both n-6 unsaturated fatty acids, play vital roles in lipopolysaccharide (LPS)-induced inflammation. The multi-functional protein scavenger receptor CD36 has also been shown to participate in inflammation. However, the molecular mechanisms underlying the interactions between CD36 and GLA or LA in LPS-induced inflammation remain unclear. We used small interfering RNA and adenoviral systems to manipulate CD36 expression in primary goat mammary gland epithelial cells (pGMECs), and the results showed that nuclear factor kappa B (NF-κB) levels were significantly decreased by CD36 receptor signaling following treatment with GLA but not LA. GLA inhibited NF-κB activation in LPS-induced pGMECs. However, silencing CD36 or deleting its fatty acid-binding domain blocked the anti-inflammatory effects of GLA, resulting in an increase in NF-κB activation and disrupting its localization during LPS-induced inflammation. The activity of the cytokines IL-1β, IL-6, and TNF-α, which act downstream of NF-κB, was also modulated when CD34 expression was manipulated by the addition of GLA in LPS-induced pGMECs. Our data suggest that GLA, but not LA, may interact with the CD36 fatty acid-binding domain to regulate the activation and localization of NF-κB in LPS-induced pGMECs.

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CD36 regulates fatty acid composition and sensitivity to insulin in 3T3-L1 adipocytes

Cited by 18 publications

References 20 publications

Human Soluble Prorenin Receptor Expressed in Adipose Tissue Improves Insulin Sensitivity and Endothelial Function in Obese Female Mice

Human Soluble Prorenin Receptor Expressed in Adipose Tissue Improves Insulin Sensitivity and Endothelial Function in Obese Female Mice

Adipose Carbonylation and Mitochondrial Dysfunction

Gamma-Linolenic Acid Suppresses NF-κΒ Signaling via CD36 in the Lipopolysaccharide-Induced Inflammatory Response in Primary Goat Mammary Gland Epithelial Cells

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