Glucose-lowering effects of orally administered superoxide dismutase in type 2 diabetic model rats

Abstract

Superoxide dismutase (SOD) is an enzyme found in most food sources, might be a candidate to reduce oxidative damage to intestinal barrier, thereby ameliorating the vicious circle between hyperglycemia and the oxidative damage. Here we report the oral administration of SOD, liposome-embedded SOD (L-SOD), and SOD hydrolysate to type 2 diabetic model rats to confirm this hypothesis. Oxidative damage severity in model rat intestine was indicated by malondialdehyde level, GSSG/GSH ratio, and antioxidant enzyme activity. The damage was significantly repaired by L-SOD. Furthermore, blood glucose and related indexes correlated well not only with oxidative damage results but also with indexes indicating physical intestinal damage such as colon density, H&E staining, immunohistochemical analysis of the tight junction proteins occludin and ZO-1 in the colon, as well as lipopolysaccharide and related inflammatory cytokine levels. The order of the magnitude of the effects of these SOD preparations was L-SOD > SOD > SOD hydrolysate. These data indicate that orally administered SOD can exhibit glucose-lowering effect via targeting the intestine of diabetic rats and systemic lipopolysaccharide influx.

Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID

“…Oral administration of liposome-embedded SOD (L-SOD) could ameliorate oxidative damage and inflammatory responses via inhibition of myeloperoxidase (MPO) and pro-inflammatory cytokines, as well as protect gut barrier function by promoting the expression of the tight junction proteins occludin and zonula occluden (ZO)-1 in the colon 750 . Furthermore, L-SOD could also reduce OxS to intestinal barrier, thereby ameliorating the vicious circle between hyperglycemia and the oxidative damage 751 . Therefore, targeting the intestinal barrier with dietary bioactive L-SOD could be a promising glucose-lowering approach to reset HMRD-induced new onset diabetes in PASC patients.…”

Liposome-embedded SOD attenuated DSS-induced ulcerative colitis in mice by ameliorating oxidative stress and intestinal barrier dysfunction

“…L-SOD was prepared by a reverse evaporation method with slight modifications according to a previous laboratory research method. 30 Briefly, 5.0 mg of SOD was thoroughly dissolved in 5.0 mL of distilled water with stirring, and then 0.25 g of soy lecithin and 0.125 g of cholesterol were dissolved in 15.0 ml of absolute ether. Subsequently, the SOD aqueous solution was mixed with the lecithin–cholesterol ether solution and sonicated at 100 W for 9 min at room temperature, with a sonication time of 5 s and intervals of 5 s to promote the self-assembly of lecithin to form liposomes to embed SOD.…”

“…Liposome-embedded SOD (L-SOD) has better stability than lecithin-modified SOD, as our previous research has shown that L-SOD can effectively resist harsh environments (gastric acid or proteases) and retain biological activities. 30 Notably, in recent research reports, SOD was encapsulated in lipid–polymer hybrid nanoparticles and showed good potential in the enema treatment of inflammatory bowel disease. Enemas usually have a short residence time in the colonic lumen, are inefficient in delivery, and have a limited therapeutic effect because they require frequent administration, resulting in low patient compliance.…”

Redox Balance in Type 2 Diabetes: Therapeutic Potential and the Challenge of Antioxidant-Based Therapy

“…Exogenous administration of AOX enzymes or their mimetics had anti-diabetic effects in cellular and rodent models [88]. Liposome-embedded SOD or SOD mimics improved glucose tolerance and insulin sensitivity in diet-induced obese mice and diabetic rats [89][90][91], attenuated the progression of diabetic nephropathy in T2D mice [92], and protected β-cells from oxidative damage [93]. Similarly, ebselen, a GPx mimic, also improved insulin sensitivity [94], preserved pancreatic β-cell function in diabetic rodents [95] and prevented diabetes-related atherosclerosis and renal damage [96].…”