Effects of Administering Sodium Selenite, Methylseleninic Acid, and Seleno-L-methionine on Glucose Tolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Mouse Model

Ueno, Hitoshi; Shimizu, Ryo; Okuno, Tomofumi; Ogino, Hirofumi; Arakawa, Takeshi; Sakazaki, Fumitoshi; Nakamuro, Katsuhiko

doi:10.1248/bpb.b14-00373

Cited by 9 publications

(6 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…32,33) Although supplementary SeMet significantly decreased plasma insulin levels in HFD groups, it had no effect for OGTT blood glucose level in HFD induced-insulin resistance. This suggests that SeMet has an insulin-mimetic action as described previously, 31) but its action may not be as significant as the suppression of blood glucose occurs.…”

Section: Discussionmentioning

confidence: 52%

“…30) These reports are inconsistent with our results, but the effect of supplementary Se on glucose tolerance or insulin resistance may be dependent on the dosage and the bioavailability of selenocompounds described previously. 27,31) The high Se dosage is reported to exacerbate insulin resistance of diabetic mouse models. 32,33) Although supplementary SeMet significantly decreased plasma insulin levels in HFD groups, it had no effect for OGTT blood glucose level in HFD induced-insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Role of Supplementary Selenium on the Induction of Insulin Resistance and Oxidative Stress in NSY Mice Fed a High Fat Diet

Murano

Ogino

Okuno

et al. 2018

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

The role of supplementary selenium on the induction of insulin resistance and oxidative stress in a diabetic mouse model was investigated in NSY mice on a high fat diet (HFD) and administered seleno-L-methionine (SeMet)-containing water for 12 weeks. Significant increases in oral glucose tolerance-tested (OGTT), insulin tolerance-tested, and non-fasting blood glucose levels were observed in mice on a HFD, as well as the significant increases in OGTT and non-fasting plasma insulin levels. Mice on a HFD had decreased plasma adiponectin levels and increased free fatty acid (FFA) levels. Supplementary SeMet significantly augmented OGTT blood glucose levels in mice on a HFD and plasma FFA levels in mice on a normal diet. The mRNA levels of six selenoproteins were measured, and glutathione peroxidase (GPx) 1 and selenoprotein P (SelP) were selected as candidates that may be associated with insulin resistance or oxidative stress in the liver. Hepatic GPx1 expression was elevated in mice on a HFD and SeMet supplementation, and SelP expression increased in mice on a HFD. Histopathological observations in hepatic tissues showed hypertrophy of parenchymal cells and significant expression of 4-hydroxy-2-nonenal in mice on a HFD, indicating lipid accumulation and oxidative stress induction. Hepatic protein tyrosine phosphatase activity also increased by a HFD. These results suggest that hepatic lipid accumulation in NSY mice on a HFD promoted oxidative stress and hepatic SelP expression, and supplementary SeMet induced hepatic GPx1 expression.Key words selenium; diabetes; insulin resistance; glutathione peroxidase 1; selenoprotein P; oxidative stress Type 2 diabetes mellitus is a metabolic disease associated with genetic and lifestyle factors 1) caused by the decline in insulin potency in organs, such as liver, muscle, and adipose tissue, and/or reduced insulin secretion from pancreatic β-cells. 2)This disease leads to diabetic peripheral neuropathy, nephropathy, and retinopathy by raising the level of blood glucose, and eventually gangrene, renal failure, and blindness.3) These pathologies are linked on an individual level to obesity and overweight, 4) on a physiological level to insulin resistance, 5) and on a cellular level to oxidative stress. 6) Insulin-resistant diabetes is a state of declined glucose uptake in target tissue cells, which do not properly respond to insulin and do not have a functioning insulin transduction system. 7) Intracellular production of reactive oxygen species (ROS) and redox activation of protein tyrosine phosphatase (PTP) 1B are involved in the decline of insulin signal transduction phosphorylation [8][9][10] and dysfunction in pancreatic β-cells. 11,12) Selenium (Se) is an essential trace element and functions as a key component of critical enzymes for redox homeostasis and protection from oxidative stress, which include the glutathione peroxidase (GPx) family and selenoprotein P (SelP). 13,14) GPx1 is located in the cytosol to remove hydrogen peroxide (H 2 O 2 ), which is generated by intrac...

show abstract

Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Role of Supplementary Selenium on the Induction of Insulin Resistance and Oxidative Stress in NSY Mice Fed a High Fat Diet

Murano

Ogino

Okuno

et al. 2018

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

show abstract

“…Selenocompound metabolism was predicted to increase by treatment with SB through PICRUSt analysis based on the 16S rRNA sequences. Selenocompounds influence diabetes through energy metabolism and oxidative stress in pancreatic islets (21,40,41). One study investigated the effects of selenocompounds on diabetes by using a nicotinamide and STZ-induced diabetes mouse model.…”

Section: E58mentioning

confidence: 99%

Combined effects of Scutellaria baicalensis with metformin on glucose tolerance of patients with type 2 diabetes via gut microbiota modulation

Shin

Choi

et al. 2020

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Metformin is a widely prescribed antidiabetic agent, whereas Scutellaria baicalensis (SB) is a commonly used medicinal herb for treatment of type 2 diabetes (T2D). Gut microbiota is involved in pathophysiology of metabolic diseases including T2D, and intestinal microbiota may be one of the important therapeutic targets for the ailment. This study was conducted to investigate the effects of SB combined with metformin on treatment of T2D while evaluating changes in the gut microbiota composition. Patients with T2D were randomized into control and treatment groups. Subjects who had already been prescribed metformin were allotted to additional SB (3.52 g/day) group or placebo group. The initial treatment session was 8 wk, and after washout period for 4 wk they were crossed over to the opposite treatment for another 8 wk. The influence of SB and placebo on the intestinal microbiota was analyzed by MiSeq system based on 16S rRNA gene. Glucose tolerance was lower in the SB group than the placebo group. Similarly, the relative RNA expression of TNF-α was significantly reduced after SB treatment. SB treatment influenced the gut microbiota, especially Lactobacillus and Akkermansia, which showed remarkable increases after SB treatment. Some subjects showed high liver enzyme levels after SB treatment, and their microbiota composition at baseline differed with subjects whose liver enzymes were not affected. We also predicted that selenocompound metabolism was increased and naphthalene degradation was decreased after SB treatment. These results suggest that SB with metformin treatment may improve the glucose tolerance and inflammation and influence the gut microbiota community in T2D.

show abstract

“…33) We previously reported that SeMet exhibited the highest bioavailability of the 3 selenocompounds supplemented under insufficient Se status, particularly in the pancreatic Se content and GPX1 activity. 24) However, as shown in Figs. 4 and 5, insulin density was not restored by SeMet ingestion, whereas 8-OHdG density in pancreatic islets significantly decreased with supplementation.…”

Section: Discussionmentioning

confidence: 91%

“…24) Briefly, ICR mice (10 mice/group) were fasted for 16 h and then intraperitoneally treated twice with 100 mg/kg STZ 15 min after an injection of 120 mg/kg NA at a 1-d interval. The next day, mice were orally administered 158 µg Se (2 µmol)/kg/d SeMet for 5 weeks with ad libitum access to sterilized water and a γ-rayirradiated torula yeast-based diet (32.3±2.92 ng Se/g) as a Sedeficient diet.…”

Section: Methodsmentioning

confidence: 99%

Effect of Seleno-L-methionine on Oxidative Stress in the Pancreatic Islets of a Short-Term Induced Diabetic Mouse Model in Insufficient Selenium Status

Ueno

Shimizu

Okuno

et al. 2018

Biological & Pharmaceutical Bulletin

Self Cite

View full text Add to dashboard Cite

The protective effects of seleno-L-methionine (SeMet) on oxidative stress in pancreatic islets were investigated with a short-term nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally injected twice with 100 mg/kg STZ and 120 mg/kg NA at a 1-d interval and were then orally administered 158 µg Se/kg SeMet with free access to a selenium-deficient diet for 5 weeks. Administration of SeMet significantly improved the levels of glycated hemoglobin (HbA1c), non-fasting and oral glucose tolerance-tested (OGTT) blood glucose, plasma adiponectin and hepatic glycogen that deteriorated by NA/STZ treatment. However, supplementary SeMet did not restore non-fasting plasma insulin levels in NA/STZ treatment group and significantly suppressed OGTT plasma insulin levels in the control group. Although SeMet significantly suppressed 8-hydroxy-2′-deoxyguanosine density in pancreatic islets, SeMet did not restore insulin density. The hepatic and pancreatic mRNA levels of glutathione peroxidase 1 (GPX1) increased by NA/STZ treatment or SeMet administration. These results suggest that although a physiological level of SeMet improves glucose tolerance by exhibiting insulin-mimetic activity in a short-term induced diabetic mouse model under insufficient Se status, the suppression of pancreatic oxidative stress with the induction GPX1 by SeMet supplementation is unlikely to restore insulin storage and secretion.Key words selenium; diabetes; insulin; glutathione peroxidase 1; seleno-L-methionine; oxidative stress Selenium (Se) is one of the essential micronutrients for human and animals and exerts as a key component of selenoproteins to regulate many physiological functions.1) The families of glutathione (GSH) peroxidase (GPX) and thioredoxin reductase (TR) are the well-known Se-dependent antioxidant enzymes.2,3) GPX1 is particularly important because the antioxidant enzyme has the higher affinity than catalase for hydrogen peroxide (H 2 O 2 ) 4) that is formed by superoxide dismutase from superoxide anions 5) or directly generated by oxidative stress in cytoplasm. Therefore, Se deficiency induces some pathological conditions including cancer and cardiovascular disease.6) The patients with Se-deficiency syndrome, Keshan disease cause cardiomyopathy with the pancreatic atrophy and degeneration.7) The fragility for the oxidative stress in pancreas may be responsible for the pathogenesis. 8)The early stages of type 2 diabetes is characterized by postprandial hyperglycemia by insufficient secretion of insulin from pancreatic β-cells and by the poor response on the target organs.9,10) As the etiology of type 2 diabetes is linked to genetic and lifestyle factors, 11,12) the onset is preventable through the improvements of dietary habits and lifestyle.13) However, deteriorations in dietary habits and lifestyle are involved with oxidative stress 14) and thereby connected with the onset of diabetes.15) Increased generation of reactive oxygen species (ROS) promotes a functional disorder in pancreat...

show abstract

Effects of Administering Sodium Selenite, Methylseleninic Acid, and Seleno-L-methionine on Glucose Tolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Mouse Model

Cited by 9 publications

References 42 publications

Role of Supplementary Selenium on the Induction of Insulin Resistance and Oxidative Stress in NSY Mice Fed a High Fat Diet

Role of Supplementary Selenium on the Induction of Insulin Resistance and Oxidative Stress in NSY Mice Fed a High Fat Diet

Combined effects of Scutellaria baicalensis with metformin on glucose tolerance of patients with type 2 diabetes via gut microbiota modulation

Effect of Seleno-L-methionine on Oxidative Stress in the Pancreatic Islets of a Short-Term Induced Diabetic Mouse Model in Insufficient Selenium Status

Contact Info

Product

Resources

About