Nano Research, Journal Year: 2024, Volume and Issue: 18(2), P. 94907082 - 94907082
Published: Dec. 27, 2024
Language: Английский
Nano Research, Journal Year: 2024, Volume and Issue: 18(2), P. 94907082 - 94907082
Published: Dec. 27, 2024
Language: Английский
Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)
Published: July 13, 2024
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia. It involves disturbances in carbohydrate, fat, and protein metabolism due to defects insulin secretion, action, or both. Novel therapeutic approaches are continuously being explored enhance control prevent complications associated with the disease. This study investigates potential of kaempherol-3-rhamnoside, flavonoid, managing diabetes modulating AMP-activated kinase (AMPK) pathway improving enzyme activities streptozotocin (STZ) -induced diabetic mice. Diabetic mice were treated varying doses kaempherol-3-rhamnoside and/or over 28-day period. Glycolytic gluconeogenesis liver, fasting blood glucose levels, serum lipid profiles oxidative stress markers assessed. Treatment significantly improved glycolytic activities, reduced glucose, enhanced levels compared controls. The compound also normalized suggesting its reversing dyslipidemia damage. Furthermore, activated AMPK pathway, indicating mechanism through which it could exert effects. Kaempherol-3-rhamnoside exhibits promising antidiabetic properties, potentially activation modulation. These findings support use as an adjunct therapy for management. Further clinical studies warranted validate these results human subjects.
Language: Английский
Citations
5bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown
Published: March 3, 2025
Abstract Background and aim Lysine is an essential amino acid with insulinotropic effects in humans. In vitro , lysine also potentiates glucose-stimulated insulin secretion (GSIS) β cell lines rodent pancreatic islets. For decades it has been assumed that action of mediated by plasma membrane depolarization similar to arginine. Aminoadipate-Semialdehyde Synthase (AASS) a mitochondrial-located bifunctional enzyme engaged the first two steps catabolism. Whether AASS-dependent catabolism occurs cells whether required for its not investigated. Methods mRNA expression pathway genes was assessed human islets from non-diabetic (ND) type 2 diabetes (T2D) subjects. AASS silenced INS1 832/13 cells. metabolism function were investigated ELISA, extracellular flux analysis, live calcium imaging, transcriptomics metabolomics analyses. Results Expression involved catabolism, including AASS, ALDH7A1, DHTKD1 HADH reduced T2D donors. Silencing resulted lysine- Surprisingly, analysis Aass -KD suppressed identified γ-aminobutyric (GABA)/glutamate ratio as well altered implicated GABA metabolism. This accompanied mitochondrial TCA cycle oxidative phosphorylation (OXPHOS) activity, reflected elevated lactate/pyruvate whole-cell ATP/ADP content ATP-linked respiration. Glucose-and GABA-stimulated cytosolic Aass-KD Strikingly, addition recovered impaired Conclusion maintain adequate shunt signaling. addition, supports energy production, uptake secretion. Reduced may contribute depletion dysfunction patients.
Language: Английский
Citations
0Mitochondrion, Journal Year: 2025, Volume and Issue: unknown, P. 102039 - 102039
Published: April 1, 2025
Language: Английский
Citations
0Acta Physiologica, Journal Year: 2025, Volume and Issue: 241(6)
Published: May 19, 2025
Language: Английский
Citations
0bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown
Published: July 2, 2024
Abstract Barth syndrome is a multisystem genetic disorder caused by mutation in TAFAZZIN , gene that encodes phospholipid:lysophospholipid transacylase important for cardiolipin remodeling. Syndrome patients suffer from number of symptoms including early heart failure, fatigue, and systemic metabolic alterations, hypoglycemia. The endocrine pancreas central to glucose homeostasis, however, the impact defective remodeling on pancreatic islet function consequences metabolism unclear. Surprisingly, mouse model with global knockdown, we observed improved tolerance compared wildtype littermates. We show secretory are robustly maintained through various compensatory mechanisms increased uptake mitochondrial volume. Transcriptomics analyses revealed expression genes encoding proteins involved N-acetylglucosamine synthesis protein O -linked N-acetylglucosaminylation. These pathways might provide molecular mechanism coupling changes volume regulation.
Language: Английский
Citations
0Nano Research, Journal Year: 2024, Volume and Issue: 18(2), P. 94907082 - 94907082
Published: Dec. 27, 2024
Language: Английский
Citations
0