Dataset Information

Oxidative status of erythrocytes, hyperglycemia, and hyperlipidemia in diabetic cats.

ABSTRACT:

Background

Erythrocytes of diabetic cats have decreased superoxide dismutase activity, possibly indicative of oxidative stress.

Hypothesis

Erythrocytes of diabetic cats undergo oxidative stress, which is caused by hyperglycemia and hyperlipidemia, and improves with treatment.

Animals

Twenty-seven client-owned cats with diabetes mellitus, 11 matched healthy cats, and 21 purpose-bred healthy cats.

Methods

Prospective study. Advanced oxidized protein products, carbonyls (protein oxidation by-products), and thiols (antioxidants) were quantified in erythrocyte membrane, thiobarbituric acid reactive substances (TBAR, lipid peroxidation by-products), and thiols in erythrocyte cytoplasm of all cats. Comparison were performed between diabetic and matched healthy cats, between diabetic cats achieving remission or not, and among purpose-bred cats after 10?days of hyperglycemia (n = 5) or hyperlipidemia (n = 6) versus controls treated with saline (n = 5) or untreated (n = 5).

Results

Compared with controls, erythrocytes of diabetic cats initially had higher median membrane carbonyls (4.6 nmol/mg total protein [range: 0.1-37.7] versus 0.7 [0.1-4.7], P Conclusions and clinical importanceDiabetes mellitus is associated with increased protein oxidation and reduced antioxidant defenses, which persist during treatment and remission, although mild improvement in protein oxidation occurs. Short-term hyperglycemia or hyperlipidemia does not cause oxidative stress. The reason for decreased TBAR remains unknown.

SUBMITTER: Zini E

PROVIDER: S-EPMC7096612 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Oxidative status of erythrocytes, hyperglycemia, and hyperlipidemia in diabetic cats.

Zini Eric E Gabai Gianfranco G Salesov Elena E Gerardi Gabriele G Da Dalt Laura L Lutz Thomas A TA Reusch Claudia E CE

Journal of veterinary internal medicine 20200216 2

<h4>Background</h4>Erythrocytes of diabetic cats have decreased superoxide dismutase activity, possibly indicative of oxidative stress.<h4>Hypothesis</h4>Erythrocytes of diabetic cats undergo oxidative stress, which is caused by hyperglycemia and hyperlipidemia, and improves with treatment.<h4>Animals</h4>Twenty-seven client-owned cats with diabetes mellitus, 11 matched healthy cats, and 21 purpose-bred healthy cats.<h4>Methods</h4>Prospective study. Advanced oxidized protein products, carbonyls ...[more]

PMID: 32064685

Similar Datasets

Project description:PurposeDiabetic retinopathy (DR) is one of the most common reasons for blindness. uncoupling protein 2 (UCP2), an uncoupling protein located in mitochondria, has been reported to be related to metabolic and vascular diseases. This research aimed to illustrate the function and mechanism of UCP2 in the pathogenesis of DR.MethodsHuman epiretinal membranes were collected to investigate the expression of UCP2 by quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence. Primary human retinal microvascular endothelial cells (HRECs) were cultured in high glucose (HG) to establish an in vitro cell model for DR. Flow cytometry analysis was used to measure intracellular reactive oxygen species (ROS). Senescence levels were evaluated by the senescence-associated beta-galactosidase (SA-β-gal) assay, the expression of senescence marker P21, and cell-cycle analysis. Adenovirus-mediated UCP2 overexpression or knockdown and specific inhibitors were administered to investigate the underlying regulatory mechanism.ResultsProliferative fibrovascular membranes from patients with DR illustrated the downregulation of UCP2 and sirtuin 3 (SIRT3) by qRT-PCR and immunofluorescence. Persistent hyperglycemia-induced UCP2 downregulation in the progress of DR and adenovirus-mediated UCP2 overexpression protected endothelial cells from hyperglycemia-induced oxidative stress and senescence. Under hyperglycemic conditions, UCP2 overexpression attenuated NAD+ downregulation; hence, it promoted the expression and activity of SIRT3, an NAD+-dependent deacetylase regulating mitochondrial function. 3-TYP, a selective SIRT3 inhibitor, abolished the UCP2-mediated protective effect against oxidative stress and senescence.ConclusionsUCP2 overexpression relieved oxidative stress and senescence based on a novel mechanism whereby UCP2 can regulate the NAD+-SIRT3 axis. Targeting oxidative stress and senescence amelioration, UCP2-SIRT3 signaling may serve as a method for the prevention and treatment of DR and other diabetic vascular diseases.

Dataset Information

Oxidative status of erythrocytes, hyperglycemia, and hyperlipidemia in diabetic cats.

Background

Hypothesis

Animals

Methods

Results

Publications

Oxidative status of erythrocytes, hyperglycemia, and hyperlipidemia in diabetic cats.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets