2018
DOI: 10.1172/jci97702
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Intracellular lipid metabolism impairs β cell compensation during diet-induced obesity

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Cited by 34 publications
(28 citation statements)
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References 65 publications
(95 reference statements)
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“…decreased GSIS in Min6 cells and murine islets) after inhibiting specific components of sphingolipid metabolism. Recently Ye et al [53] showed that during dietinduced obesity, mice with knockout of pancreatic beta cellspecific LDL receptor-related protein 1 (a pleiotropic mediator of cholesterol, insulin, energy metabolism and other cellular processes) were unable to compensate beta cell function partly due to downregulation of sphingolipid metabolism. Therefore, downregulated sphingolipid metabolism may play a causal role in pancreatic beta cell dysfunction.…”
Section: Discussionmentioning
confidence: 99%
“…decreased GSIS in Min6 cells and murine islets) after inhibiting specific components of sphingolipid metabolism. Recently Ye et al [53] showed that during dietinduced obesity, mice with knockout of pancreatic beta cellspecific LDL receptor-related protein 1 (a pleiotropic mediator of cholesterol, insulin, energy metabolism and other cellular processes) were unable to compensate beta cell function partly due to downregulation of sphingolipid metabolism. Therefore, downregulated sphingolipid metabolism may play a causal role in pancreatic beta cell dysfunction.…”
Section: Discussionmentioning
confidence: 99%
“…For example, in vitro high-glucose stimulation can induce IL-1β secretion from islets through activation of the NLRP3 inflammasome 42,43 . Circulating SFAs could also induce islet inflammation, particularly in the presence of hyperglycaemia 10,44,45 . Although circulating cytokine levels are often increased in obesity and diabetes mellitus, these cytokines serve primarily as biomarkers of systemic inflammation, as the concentration of circulating cytokines is much lower than the biologically active levels that occur within the local tissue microenvironment.…”
Section: The Initiating Factors For Islet Inflammation An Important mentioning
confidence: 99%
“…Several studies have indicated that SFAs and potentially lipoproteins are circulating factors that might contribute to islet inflammation, β-cell dysfunction and β-cell hyperplasia 10,44,45 . For example, experimental elevation of palmitate levels in mice induces islet inflammation 10 .…”
Section: Lipids As Mediators Of Crosstalkmentioning
confidence: 99%
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“…Yang et al [21] directly revealed that high glucose could induce autophagy via the mTORC1 pathway, which led to PF and ultrafiltration failure. Moreover, studies have also demonstrated that the activation of the mTORC1 pathway disrupts the intracellular cholesterol homeostasis, which results in excessive uptake of cholesterol, and ultimately exacerbation of organ injury [22,23]. To clarify the mechanisms of action by which high-glucose PDS and mTORC1 influence ECM in PMCs, we observed the intracellular lipid homeostasis.…”
Section: High-glucose Pds-mediated Activation Of Mtorc1 Contributed Tmentioning
confidence: 99%