High expression of lncRNA MALAT1 is associated with decreased insulin secretion under hyperglycemic stress in patients with type 2 diabetes mellitus

Yang, Dawei; Zhou, Lian-Ji; Huang, Qing; Ou, Linan; Wu, Biaoliang

doi:10.1007/s13410-021-00945-5

Cited by 1 publication

(4 citation statements)

References 29 publications

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“…Inflammatory situations have been closely connected to MALAT1, but no research has investigated how this lncRNA contributes to the development of the metabolic syndrome. [33][34][35] In the current study, we found a positive association between serum FBS (fast blood sugar) concentration and MALAT1 level, consistent with the results reported by Yang et al [36] This study considered that lncRNA MALAT1 might impact the body's feedback regulation of hyperglycemia, leading to more secretion of insulin to reduce the increased blood glucose. [36] In a study, Yan et al conducted a mouse model of streptozotocin induced diabetes and performed lncRNA expression profiling of retinas.…”

Section: Discussionsupporting

confidence: 92%

“…[33][34][35] In the current study, we found a positive association between serum FBS (fast blood sugar) concentration and MALAT1 level, consistent with the results reported by Yang et al [36] This study considered that lncRNA MALAT1 might impact the body's feedback regulation of hyperglycemia, leading to more secretion of insulin to reduce the increased blood glucose. [36] In a study, Yan et al conducted a mouse model of streptozotocin induced diabetes and performed lncRNA expression profiling of retinas. Results showed that lncRNAs are contributed to the pathogenesis of diabetic retinopathy via the modulation of different pathogenetic pathways.…”

Section: Discussionsupporting

confidence: 92%

“…[ 33–35 ] In the current study, we found a positive association between serum FBS (fast blood sugar) concentration and MALAT1 level, consistent with the results reported by Yang et al. [ 36 ] This study considered that lncRNA MALAT1 might impact the body's feedback regulation of hyperglycemia, leading to more secretion of insulin to reduce the increased blood glucose. [ 36 ] In a study, Yan et al.…”

Section: Discussionsupporting

confidence: 91%

“…[ 36 ] This study considered that lncRNA MALAT1 might impact the body's feedback regulation of hyperglycemia, leading to more secretion of insulin to reduce the increased blood glucose. [ 36 ] In a study, Yan et al. conducted a mouse model of streptozotocin induced diabetes and performed lncRNA expression profiling of retinas.…”

Section: Discussionmentioning

confidence: 99%

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Association between Inflammatory Factors, Vitamin D, Long Non‐Coding RNAs, MALAT1, and Adiponectin Antisense in Individuals with Metabolic Syndrome

Rashidmayvan

Khorasanchi

Nattagh‐Eshtivani

et al. 2023

Molecular Nutrition Food Res

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Background Metabolic syndrome (MetS) is a common clustering of cardiovascular risk factors associated with increased inflammation. Long non‐coding RNA (LncRNA) are involved in many of the body's metabolic activities, including inflammation. Vitamin D may play a vital role in preventing metabolic syndrome risk factors. This study aimed to evaluate the status of inflammation and expression of LncRNA and their relationship with serum vitamin D levels in patients with metabolic syndrome. Method This cross‐sectional study included staff and Mashhad University of Medical Sciences students between 30 and 50 years old who met the International Diabetes Federation criteria for Mets. Total RNA was extracted from both frozen clinical samples using the Trizol reagent. Results A total of eighty people were recruited into the two groups, with and without MetS. Inflammatory markers were higher in the individuals in the MetS group, and linear regression showed an inverse association between serum vitamin D and LncRNAs. There was a positive association between inflammatory biomarkers, lipid profiles and Adiponectin Antisense (APQ AS) expression. Conclusion APQ AS and MALAT1 levels are positively associated with inflammatory biomarkers and inverse relation between MALAT1 and serum 25 (OH) D concentration.

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