Hepatic metabolism of sulfur amino acids in db/db mice

Sulfur amino acid metabolism in Zucker diabetic fatty rats

“…The observed changes in hepatic and plasma sulfur amino acids and their metabolites are similar to our previous findings in db/db mice [6], with the exception of hepatic levels of SAM, SAH, and polyamines. We observed lower SAM and SAH and greater putrescine in db/db mice.…”

“…Homocysteine, GSH, and cysteine in the plasma and liver were quantified using the SBD-F method [6]. For sample preparation, 10 mL of 10 mM MPG was used as an internal standard, and was added to 50 mL sample.…”

“…Both BHMT and MS activities were estimated by quantifying the formation of methionine [6]. For BHMT, the reaction mixtures (final volume 150 mL) consisted of 50 mM potassium phosphate buffer (PPB, pH 7.4) containing 2.5 mM betaine, 7 mM homocysteine and 1 mg protein/mL.…”

“…Our previous studies showed that changes in plasma homocysteine level in obese or diabetic conditions were dependent on the type of experimental animal model used [6][7][8]. Plasma total homocysteine concentration increased by 1.6-fold in obese mice fed a high-fat diet for 12 weeks [7], but was 40% lower in db/ db mice, obese type 2 diabetic animals with a G-to-T point mutation of the leptin receptor [6]. In contrast, plasma homocysteine levels were similar between control rats and non-obese type diabetic Goto-Kakizaki rats [8].…”

Genome-scale transcriptional analysis reveals key genes associated with the development of type II diabetes in mice

“…Db/db mice were discovered by Hummel et al in the inbred line of C57BLKS/J (BKS) in 1966, which is caused by mutations in the gene of leptin receptor (Lepr) gene located in mouse chromosome 4 (7). In db/db mice this typically presents as a hypothalamic defect; wherein satiety is not produced due to a lack of the satiety substance (leptin), lack of reaction to anabolic greater than catabolism, and gradually develop severe T2D accompanied by hyperglycemia due to the accumulation of fat (8) Mice and humans with T2D exhibit similar clinical symptoms, such as polydipsia, polyphagia, urorrhagia, obesity, hyperglycemia, hyperglycemia, IR and lipid metabolism abnormality (9). Using the db/db mice model, it may be possible to investigate the underlying molecular mechanisms and elucidate the complex intrinsic metabolic processes associated with T2D.…”