Correction: Application of carbon-based nanomaterials in Alzheimer's disease.

Correction for 'Application of carbon-based nanomaterials in Alzheimer's disease' by Mengyao Bai , , 2024, https://doi.org/10.1039/D4MH01256A.

Application of carbon-based nanomaterials in Alzheimer's disease.

Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disorder marked by permanent impairment of brain function across the whole brain. This condition results in a progressive deterioration of cognitive function in patients and is frequently associated with psychological symptoms such as agitation and anxiety, imposing a significant burden on both patients and their families. Nanomaterials possess numerous distinctive physical and chemical features that render them extensively utilized.

Novel photocatalytic carbon dots: efficiently inhibiting amyloid aggregation and quickly disaggregating amyloid aggregates.

Amyloid aggregation is implicated in the pathogenesis of various neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease (PD). It is critical to develop high-performance drugs to combat amyloid-related diseases. Most identified nanomaterials exhibit limited biocompatibility and therapeutic efficacy.

Calycosin-7-O-β-D-glucoside attenuates palmitate-induced lipid accumulation in hepatocytes through AMPK activation.

Calycosin-7-O-β-D-glucoside (CG) is the major component of Astragali Radix (AR), a traditional Chinese drug. As reported, CG could attenuate cerebral ischemia/reperfusion injury, protect blood-brain barrier integrity, and ameliorate myocardial infarction. To date, whether CG has a protective effect on metabolic diseases remains to be elucidated.

SIRT2 ablation inhibits glucose-stimulated insulin secretion through decreasing glycolytic flux.

Sirtuins are NAD-dependent protein deacylases known to have protective effects against age-related diseases such as diabetes, cancer, and neurodegenerative disease. SIRT2 is the only primarily cytoplasmic isoform and its overall role in glucose homeostasis remains uncertain. SIRT2-knockout (KO) rats were constructed to evaluate the role of SIRT2 in glucose homeostasis.

Leonurine protects against dexamethasone-induced cytotoxicity in pancreatic β-cells via PI3K/Akt signaling pathway.

Glucocorticoid excess induces pancreatic β-cell apoptosis and insulin secretion impairment, which may lead to hyperglycemia and steroid diabetes. Leonurine is a natural alkaloid extracted from the Herba leonuri, which has been widely used in the treatment of obstetric and gynecological diseases. However, whether leonurine performs a protective role in pancreatic β-cells remains unknown.

Butyrate stimulates hepatic gluconeogenesis in mouse primary hepatocytes.

Butyrate is a major short-chain fatty acid (SCFA) produced by microbial fermentation of dietary fiber in the gastrointestinal tract. Butyrate is also a well-known broad-spectrum histone deacetylase (HDAC) inhibitor. Butyrate has been reported to improve energy metabolism in rodents, which is associated with its beneficial effects on skeletal muscle, brown fat tissue and pancreatic β-cells.

The pivotal role of protein acetylation in linking glucose and fatty acid metabolism to β-cell function.

Protein acetylation has a crucial role in energy metabolism. Here we performed the first large-scale profiling of acetylome in rat islets, showing that almost all enzymes in core metabolic pathways related to insulin secretion were acetylated. Label-free quantitative acetylome of islets in response to high glucose revealed hyperacetylation of enzymes involved in fatty acid β-oxidation (FAO), including trifunctional enzyme subunit alpha (ECHA).

Role of hepatic neuregulin 4 in the regulation of gluconeogenesis in mice.

Aims: Enhanced hepatic gluconeogenesis is an important cause of hyperglycemia in type 2 diabetes. However, the regulatory mechanisms underlying disordered hepatic gluconeogenesis remains largely unclear. In the present study, we investigated the potential role of hepatic neuregulin 4 (Nrg4) in the regulation of gluconeogenesis in mice.

Berberine inhibits glucose oxidation and insulin secretion in rat islets.

Glucose promotes insulin secretion primarily via its metabolism and the production of metabolic coupling factors in beta-cells. The activation of AMP-activated protein kinase (AMPK), an energy sensor, results in a decrease in insulin secretion from beta-cells, but its mechanism remains largely unknown. Berberine, an oral anti-diabetic drug, has been shown to activate AMPK in multiple peripheral tissues.

Berberine-induced activation of AMPK increases hepatic FGF21 expression via NUR77.

Fibroblast growth factor 21 (FGF21), a hormone-like protein mainly derived from liver, exhibits multiple beneficial effect on energy metabolism. Similar to FGF21, berberine exerts anti-hyperglycemic and anti-dyslipidemic properties. Previous studies revealed that the beneficial metabolic effect of berberine was attributed to the activation of AMP-activated protein kinase (AMPK).

Glucose enhances rat islet function via stimulating CART expression.

Cocaine- and amphetamine-regulated transcript (CART) is an anorexigenic peptide widely expressed in the central and peripheral nervous systems, as well as in endocrine cells. CART is markedly upregulated in the β-cells of several rodent models of type-2 diabetes. The stimulatory effect of exogenous CART peptide on insulin secretion is cAMP dependent.

Potential role of Hsp90 in rat islet function under the condition of high glucose.

Aims: The preservation of pancreatic β-cell function is a key point in the treatment of type 2 diabetes mellitus. There is substantial evidence demonstrating that heat-shock protein 90 (Hsp90) is needed for the stabilization and correct folding of client proteins and plays important roles in various biological processes. Here, we revealed the important role of Hsp90 in β-cell function.