Chronic exposure of glucose rich environment creates several physiological and pathophysiological changes. There are several pathways by which hyperglycemia exacerbate its toxic effect on cells, tissues and organ systems. Hyperglycemia can induce oxidative stress, upsurge polyol pathway, activate protein kinase C (PKC), enhance hexosamine biosynthetic pathway (HBP), promote the formation of advanced glycation end-products (AGEs) and finally alters gene expressions. Prolonged hyperglycemic condition leads to severe diabetic condition by damaging the pancreatic β-cell and inducing insulin resistance. Numerous complications have been associated with diabetes, thus it has become a major health issue in the 21st century and has received serious attention. Dysregulation in the cardiovascular and reproductive systems along with nephropathy, retinopathy, neuropathy, diabetic foot ulcer may arise in the advanced stages of diabetes. High glucose level also encourages proliferation of cancer cells, development of osteoarthritis and potentiates a suitable environment for infections. This review culminates how elevated glucose level carries out its toxicity in cells, metabolic distortion along with organ dysfunction and elucidates the complications associated with chronic hyperglycemia.
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http://dx.doi.org/10.1016/j.biopha.2018.07.157 | DOI Listing |
Int J Biol Macromol
January 2025
College of Marine and Bioengineering, Yancheng Institute of Technology, Yancheng 224051, China. Electronic address:
Type 2 diabetes mellitus (T2DM) represents a chronic metabolic disorder characterized by disrupted carbohydrate and lipid balance, resulting in hyperglycemia. This study evaluated the impact of polysaccharides derived from Cynanchum auriculatum Royle ex Wight (CRP) on mitigating hyperglycemia and modulating intestinal microbiota in T2DM mice. Findings indicated that CRP is mainly linked by →6)α-D-Glcp-(1→ and CRP-H demonstrated greater efficacy than CRP-L in regulating hypoglycemic-related indicators such as serum high-density lipoprotein cholesterol (HDL-c) level.
View Article and Find Full Text PDFJ Steroid Biochem Mol Biol
January 2025
Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Medicine, VA Medical Center, St. Louis, MO, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address:
Targeting optimal glycemic control based on hemoglobin A1c (A1c) values reduces but does not abolish the onset of diabetic kidney disease and its progression to chronic kidney disease (CKD). This suggests that factors other than the average glucose contribute to the residual risk. Vitamin D deficiency and frequent episodes of acute hyperglycemia (AH) are associated with the onset of albuminuria and CKD progression in diabetes.
View Article and Find Full Text PDFJ Endocr Soc
January 2025
Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Division of Endocrinology, Diabetes and Metabolism, Long Island Jewish Medical Center, Northwell Health, New Hyde Park, NY 11040, USA.
Sodium-glucose cotransporter 2 inhibitors (SGLT2is), originally approved by the US Food and Drug Administration for glycemic control in type 2 diabetes mellitus (DM2), have shown substantial cardiovascular and renal benefits, leading to their expanded use in managing heart failure (HF) and chronic kidney disease in the outpatient setting. Despite these benefits, their use for inpatient hyperglycemia management is not universally endorsed due to safety concerns and inadequate data. However, emerging evidence suggests potential advantages of initiating SGLT2i treatment for patients during hospitalization in the setting of HF.
View Article and Find Full Text PDFTissue Cell
January 2025
Department of Endocrinology, Fuyang Cancer Hospital, Fuyang, Anhui Province 236000, PR China. Electronic address:
Background: Diabetes mellitus (DM), a chronic metabolic disease, is characterized by long-term hyperglycemia resulting from the defect of insulin production and insulin resistance. The damage and dysfunction of pancreatic β-cells is a main link in DM development.
Methods: In this work, pancreatic β-cell line INS-1E cells were exposed to 30 mM glucose for 48 h to construct an in vitro DM model.
Diabetes Obes Metab
January 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Taiyuan, China.
Metabolic syndrome-related diseases frequently involve disturbances in skeletal muscle lipid metabolism. The accumulation of lipid metabolites, lipid-induced mitochondrial stress in skeletal muscle cells, as well as the inflammation of adjacent adipose tissue, are associated with the development of insulin resistance and metabolic dysfunction. Consequently, when antidiabetic medications are used to treat various chronic conditions related to hyperglycaemia, the impact on skeletal muscle lipid metabolism should not be overlooked.
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