Disorders of uric acid metabolism in rats with fructose-induced experimental insulin resistance syndrome

Shuprovych, AA; Hurina, NM; Корпачева-Зиныч, О В

doi:10.15407/fz57.01.072

Cited by 10 publications

(10 citation statements)

References 14 publications

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“…In addition, fructose can reduce renal excretion of uric acid due to increased lactate production. The latter one is a competitive inhibitor of uric acid reabsorption in the renal tubules [7]. As a result of the experiment, animals of this group were determined an increase of uric acid contents in males and females at 50.6% and 36.4%, respectively (p 1-4 <0.05) as for the control, which may be due to hyperinsulinemia, which stimulates uric acid reabsorption in the tubules of the kidneys.…”

Section: Resultsmentioning

confidence: 99%

“…The studies were performed using non-pedigree mature rats weighing 150-230 g, which were divided into the following groups: group I -control (intact animals, 12 males and 12 females), groups II and III -comparison groups: group II -animals with congenital iodine deficiency (20 males and 20 females), group III -animals with acquired iodine deficiency (20 males and 20 females), group IV -animals that were under the conditions of high fructose feeding with adequate iodine supply (20 males and 20 females), group V -animals with fructose-induced insulin resistance and congenital iodine deficiency (20 males and 20 females), group VI -animals with fructose-induced insulin resistance and acquired iodine deficiency (20 males and 20 females). Animals of the experimental groups IV-VI followed the high-fructose diet (20% fructose solution) during 8 weeks [7,8]. Animals of the experimental groups II, III, V and VI followed the iodine-deficient diet, in particular; animals of the groups II and V -followed such a diet in the second generation; animals of the groups III and VI -followed it for 45 days of the experiment [4].…”

Section: Methodsmentioning

confidence: 99%

“…The development of insulin resistance and diabetes mellitus is associated with alimentary factors, among which the consumption of dietary fructose and sucrose is very important [1,2,7]. Fructose is known to cause the development of metabolic syndrome associated with the increase of body weight (development of abdominal obesity) and increased glucose tolerance [3,9].…”

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confidence: 99%

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Peculiarities of Metabolism of Rats with Fructose-induced Insulin Resistance Against the Background of Congenital and Acquired Iodine Deficiency

Stetseviat

2019

Galician med. j.

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Animals following a high-fructose diet during eight weeks, have experienced changes in metabolism and the signs of insulin resistance have developed. Under such conditions, moderate hyperglycemia, hyperinsulinemia, hyperuricemia, an increase of the level of glycosylated hemoglobin in whole blood were observed. The significant role of the HOMA-IR index, as an early marker of carbohydrate metabolism disorders at the stage of pre-diabetes, has been confirmed. In experimental animals against the background of the high-fructose diet, the changes in the lipid spectrum of the blood were revealed: an increase of the total cholesterol level, low-density lipoproteins, triglycerides against the background of a high-density lipoproteins decrease. These disorders and a significant increase of the atherogenicity reflect the development of secondary dyslipidemia. In this case, the disorders of carbohydrate metabolism were combined with the degree of dyslipidemia. Males were found to have at increased risk of development the insulin resistance and comorbid pathology. Iodine deficiency, especially of congenital nature, is an aggravating factor of metabolic disorders. The obtained data can serve as a basis for extend of preventive measures and identification of the priority treatment schemes for type 2 diabetes mellitus in residents of endemic regions.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Peculiarities of Metabolism of Rats with Fructose-induced Insulin Resistance Against the Background of Congenital and Acquired Iodine Deficiency

Stetseviat

2019

Galician med. j.

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“…The study was carried on male rats weighing 150-180 g. Rats were divided into experimental and control groups. The animals of experimental group (IR, n = 30) received 10% fructose solution instead of drinking water for eight weeks [9]. Rats of the control group (n = 30) were kept on a standard diet, normal temperature and light regime.…”

Section: Methodsmentioning

confidence: 99%

The features of metabolism and structural organization of dental system under conditions of experimental insulin resistance

Guranych¹,

Bagriy²,

Guranych³

et al. 2021

Fiziol Zh

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Peculiarities of calcium homeostasis, the activity of energy synthesis enzymes and structural organization of the dental system in rats under conditions of insulin resistance were analyzed. It was found that impaired glucose tolerance is manifested by a decreased mineralizing ability of hard tissues of alveolar processes and teeth, accompanied by a decrease in calcium content in erythrocyte mass and alveolar processes and an increase in acid phosphatase activity in blood serum. In rats with insulin resistance a decrease in the activity of lactate- and succinate dehydrogenase was detected. Degenerative changes were observed in the bone thickness of the dental area of insulin resistant rats, which were accompanied by the development of hypercellularity of the osteogenic layer of periosteum. Reactive changes in the tooth pulp were manifested by a decrease in the area of its loose connective tissue. Hyperplastic changes with the formation of unexpressed acanthotic bands developed in the oral mucosa of experimental animals, the thickness of the basal and granular layers increased against the background of a decrease in the prickle layer of epitheliocytes. In experimental group we observed a decrease in the nuclear cytoplasmic index and an increase in keratin formation in the epithelium. A narrowing of the lumen of capillaries and arterioles of the dental area, hyperplasia of endothelial cells and an increased accumulation of glycoproteins, especially in small arteries, were also detected in experimental group. Thus, altered carbohydrate metabolism leads to the metabolic changes of teeth supporting apparatus and oral mucosa, aggravating the course of insulin resistance with the development of dental system pathology.

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“…Дослідження проведені на 90 щурах-самицях масою 150-180 г, які були розділені на три дослідні та контрольну групи по 30 тварин у кожній. До 1-ї дослідної групи ввійшли щури з йододефіцитом, який відтворювали двомісячним утриманням тварин на дієті з обмеженим надходженням йоду [12]; до 2-ї -щури з інсулінорезистентністю, яку моделювали додаванням до питної води тварин 10 %-го розчину фруктози впродовж 8 тиж [13]; до 3-ї -щури з інсулінорезистентністю на тлі йододефіциту. До контрольної групи ввійшли інтактні тварини, яких утримували в умовах стандартного харчового раціону, звичайного температурного та світлового режиму віварію.…”

Section: методикаunclassified

The Changes of Mineral Density of Dento-Maxillary System of Rats With Iodine Deficiency and Insulin Resistance

Guranych¹,

Voronych-Semchenko²,

Guranych³

2018

Fiziol Zh

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Проаналізовано зміни показників активності ферментів біоенергетичних процесів, макро-та мікроелементного статусу щурів із йододефіцитом та інсулінорезистентністю. Установлено, що розвиток йододефіциту супроводжувався пригніченням активності лактатдегідрогенази (ЛДГ), лужної фосфатази (ЛФ) на тлі зростання активності кислої фосфатази (КФ), зменшенням вмісту кальцію та магнію у твердих тканинах зубів і кісток щодо значень у інтактних тварин. За умов інулінорезистентності знизилась активність сукцинатдегідрогенази (СДГ) і ЛДГ на тлі активації малатдегідрогенази (МДГ) та КФ, зменшився вміст кальцію та магнію у твердих тканинах зубів й альвеолярних відростках, збільшився вміст цинку в зубах. За умов йододефіциту пригнічувалась активність остеобластів, тоді як інсулінорезистентність більшою мірою активувала остеокласти. У щурів із інсулінорезистентністю на тлі йододефіциту суттєво зменшувалась активність дегідрогеназ сироватки крові (на 90,38-97,12 %). У еритроцитарній масі, зубах і альвеолярних відростках зменшився вміст кальцію, магнію та марганцю на 20,26-88,26 % із одночасним збільшенням вмісту цинку в тканинах зубів на 77,35 %. Порушення кальцієвого гомеостазу збігається зі зростанням активності КФ (у 2,42 раза), що може бути причиною підвищеної демінералізації зубів і кісток при поєднанні інсулінорезистентності та йододефіциту. Визначення активності ферментів біоенергосинтезу (СДГ, ЛДГ) за умов ендокринопатій можна використовувати як один із ранніх маркерів субклітинних метаболічних розладів утворення макроергів. Зміни ферментативної активності КФ і ЛФ відображають перебіг процесів регенерації кісткової тканини, що дає змогу виявити порушення мінералізації твердих тканин на ранніх етапах розвитку інсулінорезистентності та йододефіциту. Ключові слова: йододефіцит; інсулінорезистентність; ферменти енергосинтезу; макро-та мікроелементний статус.

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Disorders of uric acid metabolism in rats with fructose-induced experimental insulin resistance syndrome

Cited by 10 publications

References 14 publications

Peculiarities of Metabolism of Rats with Fructose-induced Insulin Resistance Against the Background of Congenital and Acquired Iodine Deficiency

Peculiarities of Metabolism of Rats with Fructose-induced Insulin Resistance Against the Background of Congenital and Acquired Iodine Deficiency

The features of metabolism and structural organization of dental system under conditions of experimental insulin resistance

The Changes of Mineral Density of Dento-Maxillary System of Rats With Iodine Deficiency and Insulin Resistance

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