Effects of RIPC on the Metabolomical Profile during Lower Limb Digital Subtraction Angiography: A Randomized Controlled Trial

Kuusik, Karl; Kasepalu, Teele; Zilmer, Mihkel; Eha, Jaan; Paapstel, Kaido; Kilk, Kalle; Rehema, Aune; Kals, Jaak

doi:10.3390/metabo13070856

Cited by 1 publication

(1 citation statement)

References 39 publications

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“…Moreover, PC also contributes to the transformation of brown-like adipocytes [33], which supported our results that the PC was up-regulated with the browning of mammary fat along with an increase in the BAT index in the CL316243 group. PC, composed of glycerol backbone, long-chain fatty acids, phosphate groups, and choline molecules, is also involved in the proliferative growth of mammary epithelial cells [34]. The long-chain fatty acids could be transported and absorbed by the mammary gland via circulation, thus subsequently consuming the phosphatidylcholine [35,36].…”

Section: Discussionmentioning

confidence: 99%

Browning of Mammary Fat Suppresses Pubertal Mammary Gland Development of Mice via Elevation of Serum Phosphatidylcholine and Inhibition of PI3K/Akt Pathway

Lang,

Zheng,

Liang

et al. 2023

IJMS

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Mammary fat plays a profound role in the postnatal development of mammary glands. However, the specific types (white, brown, or beige) of adipocytes in mammary fat and their potential regulatory effects on modulating mammary gland development remain poorly understood. This study aimed to investigate the role of the browning of mammary fat on pubertal mammary gland development and explore the underlying mechanisms. Thus, the mammary gland development and the serum lipid profile were evaluated in mice treated with CL316243, a β3-adrenoceptor agonist, to induce mammary fat browning. In addition, the proliferation of HC11 cells co-cultured with brown adipocytes or treated with the altered serum lipid metabolite was determined. Our results showed that the browning of mammary fat by injection of CL316243 suppressed the pubertal development of mice mammary glands, accompanied by the significant elevation of serum dioleoylphosphocholine (DOPC). In addition, the proliferation of HC11 was repressed when co-cultured with brown adipocytes or treated with DOPC. Furthermore, DOPC suppressed the activation of the PI3K/Akt pathway, while the DOPC-inhibited HC11 proliferation was reversed by SC79, an Akt activator, suggesting the involvement of the PI3K/Akt pathway in the DOPC-inhibited proliferation of HC11. Together, the browning of mammary fat suppressed the development of the pubertal mammary gland, which was associated with the elevated serum DOPC and the inhibition of the PI3K/Akt pathway.

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