Lipid transfer proteins and instructive regulation of lipid kinase activities: Implications for inositol lipid signaling and disease

Lete, Marta G.; Tripathi, Ashutosh; Chandran, Vijay; Bankaitis, Vytas A.; McDermott, Mark I.

doi:10.1016/j.jbior.2020.100740

Cited by 12 publications

(17 citation statements)

References 242 publications

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“…The MI is a precursor of inositol phosphates and is a vital second messenger signaling molecule in cellular processes, such as lipid signaling, glucose, and insulin metabolism [11,29]. The results in the current study suggest that MI can affect the lipid synthesis and metabolism in the body, thereby relieving lipid accumulation in body [16,30,31]. The qPCR results showed that dietary MI supplementation could down-regulate the expression of genes related with lipid synthesis (FAS) and up-regulate the expression of genes (CPT, PPAR-α, ATGL) related with lipid metabolism.…”

Section: Discussionmentioning

confidence: 59%

Alleviation of the Adverse Effect of Dietary Carbohydrate by Supplementation of Myo-Inositol to the Diet of Nile Tilapia (Oreochromis niloticus)

Zhu

Pan

Wang

et al. 2020

Animals

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This study investigated the effect of dietary myo-inositol (MI) on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia (Oreochromis niloticus). Six diets contained either low carbohydrate (LC 30%) or high carbohydrate (HC 45%) with three levels of MI supplementation (0, 400 and 1200 mg/kg diet) to each level of the carbohydrate diet. After an 8-week trial, the fish fed 400 mg/kg MI under HC levels had the highest weight gain and fatness, but the fish fed 1200 mg/kg MI had the lowest hepatosomatic index, visceral index and crude lipid in the HC group. The diet of 1200 mg/kg MI significantly decreased triglyceride content in the serum and liver compared with those fed the MI supplemented diets regardless of carbohydrate levels. Dietary MI decreased triglyceride accumulation in the liver irrespective of carbohydrate levels. The content of malondialdehyde decreased with increasing dietary MI at both carbohydrate levels. Fish fed 1200 mg/kg MI had the highest glutathione peroxidase, superoxide dismutase, aspartate aminotransferase and glutamic-pyruvic transaminase activities. The HC diet increased the mRNA expression of key genes involved in lipid synthesis (DGAT, SREBP, FAS) in the fish fed the diet without MI supplementation. Dietary MI significantly under expressed fatty acid synthetase in fish fed the HC diets. Moreover, the mRNA expression of genes related to lipid catabolism (CPT, ATGL, PPAR-α) was significantly up-regulated with the increase of dietary MI levels despite dietary carbohydrate levels. The gene expressions of gluconeogenesis, glycolysis and MI biosynthesis were significantly down-regulated, while the expression of the pentose phosphate pathway was up-regulated with the increase of MI levels. This study indicates that HC diets can interrupt normal lipid metabolism and tend to form a fatty liver in fish. Dietary MI supplement can alleviate lipid accumulation in the liver by diverging some glucose metabolism into the pentose phosphate pathway and enhance the antioxidant capacity in O. niloticus.

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Section: Discussionmentioning

confidence: 59%

Alleviation of the Adverse Effect of Dietary Carbohydrate by Supplementation of Myo-Inositol to the Diet of Nile Tilapia (Oreochromis niloticus)

Zhu

Pan

Wang

et al. 2020

Animals

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“…Pitpna activity represents an interesting target for miR-375 control as it is an established mediator of PtdIns-4-P synthesis within the mammalian TGN (Lete et al ., 2020; Xie et al ., 2018), and PtdIns-4-P is required for the recruitment of budding factors and secretory granule formation (Cruz-Garcia et al, 2013). Further evidence in support of Pitpna expression being a physiologically relevant miR-375 target in beta-cells was provided by quantitative liquid chromatography-tandem mass spectrometry (LC/MSMS) analyses of the MIN6 murine insulinoma cell line lipidome as a function of Pitpna expression.…”

Section: Resultsmentioning

confidence: 99%

“…Phosphatidylinositol transfer proteins (PITPs) are highly conserved molecules that regulate the interface between lipid metabolism and cellular functions (Bankaitis et al, 2010; Cleves et al, 1991). PITPs promote the activity of phosphatidylinositol (PtdIns) 4-OH kinases and PtdIns-4 phosphate (PtdIns-4-P) synthesis in eukaryotic cells (Ashlin et al, 2021; Lete et al, 2020; Xie et al, 2018). There are at least three soluble PITPs expressed in mammals -- PITPα/PITPNA, PITPβ/PITPNB, and rdgBβ/PITPnc1 (Dickeson et al, 1989; Fullwood et al, 1999; Tanaka and Hosaka, 1994).…”

Section: Introductionmentioning

confidence: 99%

Restoration of PITPNA in Type 2 diabetic human islets reverses pancreatic beta-cell dysfunction

Yeh¹,

Sona²,

Yan

et al. 2022

Preprint

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Defects in insulin processing and granule maturation are linked to pancreatic beta-cell failure during type 2 diabetes (T2D). Phosphatidylinositol transfer protein alpha (PITPNA) stimulates activity of phosphatidylinositol (PtdIns) 4-OH kinase to produce sufficient PtdIns-4-phosphate (PtdIns-4-P) in the trans-Golgi network to promote insulin granule maturation. PITPNA in beta-cells of T2D human subjects is markedly reduced suggesting its depletion accompanies beta-cell dysfunction. Conditional deletion of Pitpna in the beta-cells of Ins-Cre;Pitpnaflox/flox mice leads to hyperglycemia resulting from decreased glucose-stimulated insulin secretion (GSIS) and reduced pancreatic beta-cell mass. Furthermore, PITPNA silencing in human islets confirmed its role in PtdIns-4-P synthesis and led to impaired insulin granule maturation and docking, GSIS, and proinsulin processing with evidence of ER stress. Restoration of PITPNA in islets of T2D human subjects reversed these beta-cell defects and identify PITPNA as a critical target linked to beta-cell failure in T2D.

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“…However, a debate still exists on whether Sec14p exchanges lipids between organelles in yeast. As proposed for Sec14p, rather than transporting lipids, MOSPD2 could act by presenting its lipid substrate to an enzyme and thus increase its activity (Lete et al , 2020). Further work will be needed to determine if MOSPD2 mediates lipid transport at the ER/LD interface.…”

Section: Discussionmentioning

confidence: 99%

MOSPD2 a new endoplasmic reticulum-lipid droplet tether functioning in LD homeostasis

Zouiouich

Mattia

Martinet

et al. 2022

Preprint

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Membrane contact sites between organelles are organized by protein bridges. Among the components of these contacts, the VAP family comprises endoplasmic reticulum (ER)-anchored proteins, such as MOSPD2, functioning as major ER-organelle tethers. MOSPD2 distinguishes itself from the other members of the VAP family by the presence of a CRAL-TRIO domain. In this study, we show that MOSPD2 forms ER-LD contacts thanks to its CRAL-TRIO domain. MOSPD2 ensures the attachment of the ER to LDs through a direct protein-membrane interaction involving an amphipathic helix that has an affinity for lipid packing defects present at the surface of LDs. Remarkably, the absence of MOSPD2 markedly disturbs the assembly of lipid droplets. These data show that MOSPD2, in addition to being a general ER receptor for inter-organelle contacts, possesses an additional tethering activity and is specifically implicated in the biology of LDs via its CRAL-TRIO domain.

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Lipid transfer proteins and instructive regulation of lipid kinase activities: Implications for inositol lipid signaling and disease

Cited by 12 publications

References 242 publications

Alleviation of the Adverse Effect of Dietary Carbohydrate by Supplementation of Myo-Inositol to the Diet of Nile Tilapia (Oreochromis niloticus)

Alleviation of the Adverse Effect of Dietary Carbohydrate by Supplementation of Myo-Inositol to the Diet of Nile Tilapia (Oreochromis niloticus)

Restoration of PITPNA in Type 2 diabetic human islets reverses pancreatic beta-cell dysfunction

MOSPD2 a new endoplasmic reticulum-lipid droplet tether functioning in LD homeostasis

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