Inhibition of Amino Acids Influx into Proximal Tubular Cells Improves Lysosome Function in Diabetes.

Key Points: Collectrin serves as a chaperone for the trafficking of neutral amino acid (AA) transporters in the apical membranes of proximal tubular cells (PTCs). knockout reduced AAs influx into PTCs, inactivated mTOR, activated transcription factor EB, improved lysosome function, and ameliorated vacuolar formation of PTCs in diabetic mice treated with streptozotocin and high-fat diet. The inhibition of neutral AA transporter, such as BAT1 (SLC6A19), and transcription factor EB activator is a new therapeutic strategy against diabetic kidney disease.

Role of glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 in hypertriglyceridemia and diabetes.

In diabetes, the impairment of insulin secretion and insulin resistance contribute to hypertriglyceridemia, as the enzymatic activity of lipoprotein lipase (LPL) depends on insulin action. The transport of LPL to endothelial cells and its enzymatic activity are maintained by the formation of lipolytic complex depending on the multiple positive (glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 [GPIHBP1], apolipoprotein C-II [APOC2], APOA5, heparan sulfate proteoglycan [HSPG], lipase maturation factor 1 [LFM1] and sel-1 suppressor of lin-12-like [SEL1L]) and negative regulators (APOC1, APOC3, angiopoietin-like proteins [ANGPTL]3, ANGPTL4 and ANGPTL8). Among the regulators, GPIHBP1 is a crucial molecule for the translocation of LPL from parenchymal cells to the luminal surface of capillary endothelial cells, and maintenance of lipolytic activity; that is, hydrolyzation of triglyceride into free fatty acids and monoglyceride, and conversion from chylomicron to chylomicron remnant in the exogenous pathway and from very low-density lipoprotein to low-density lipoprotein in the endogenous pathway.

Circulating GPIHBP1 levels and microvascular complications in patients with type 2 diabetes: A cross-sectional study.

Background: Glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) plays a crucial role in lipolytic processing. Previous studies have shown that GPIHBP1 mutations cause severe hypertriglyceridemia and that serum GPIHBP1 levels are marginally higher in patients with coronary heart disease; however, the role of GPIHBP1 in type 2 diabetes mellitus (T2DM) remains unknown.

Objective: We investigated the association between circulating GPIHBP1 levels and the prevalence of microvascular complications in T2DM.

The Association of Postprandial Triglyceride Variability with Renal Dysfunction and Microalbuminuria in Patients with Type 2 Diabetic Mellitus: A Retrospective and Observational Study.

Objective: We examined whether or not day-to-day variations in lipid profiles, especially triglyceride (TG) variability, were associated with the exacerbation of diabetic kidney disease.

Methods: We conducted a retrospective and observational study. First, 527 patients with type 2 diabetes mellitus (DM) who had had their estimated glomerular filtration rate (eGFR) checked every 6 months since 2012 for over 5 years were registered.

Adipocyte-Specific Inhibition of Ameliorates Diet-Induced Obesity Through Targeting .

MicroRNAs expressed in adipocytes are involved in transcriptional regulation of target mRNAs in obesity, but miRNAs critically involved in this process is not well characterized. Here, we identified upregulation of miR-221-3p and miR-222-3p in the white adipose tissues in C57BL/6 mice fed with high fat-high sucrose (HFHS) chow by RNA sequencing. and are paralogous genes and share the common seed sequence and mice fed with HFHS chow demonstrated resistance to the development of obesity compared with .

Corrigendum: Upregulation of in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control.

[This corrects the article DOI: 10.3389/fendo.2021.

Corrigendum: Upregulation of Mir342 in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control.

[This corrects the article DOI: 10.3389/fendo.2021.

Upregulation of in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control.

In obesity and type 2 diabetes, numerous genes are differentially expressed, and microRNAs are involved in transcriptional regulation of target mRNAs, but miRNAs critically involved in the appetite control are not known. Here, we identified upregulation of miR-342-3p and its host gene in brain and adipose tissues in C57BL/6 mice fed with high fat-high sucrose (HFHS) chow by RNA sequencing. (-/-) mice fed with HFHS chow were protected from obesity and diabetes.