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Betaine is a biologically active compound exerting beneficial effects in the organism, however, the exact mechanisms underlying its action are not fully elucidated. The present study aimed to explore, whether betaine alleviates disorders induced by feeding rats a high-fat diet (HFD). Rats were divided into 3 groups: control, fed an HFD and fed an HFD and receiving betaine (2% water solution for 8 weeks). Betaine improved glucose tolerance, decreased blood levels of non-esterified fatty acids and prevented lipid accumulation in the skeletal muscle of rats on an HFD. Betaine reduced activities of blood alanine aminotransferase, blood levels of bilirubin and hepatic lipid content. Expression of fatty acid synthase in the liver and the skeletal muscle was decreased in response to feeding an HFD, and this effect was deepened by betaine in the muscle tissue. Hepatic and muscular expression of genes related to insulin signaling were unchanged in HFD-fed rats. Lipolysis stimulated by epinephrine (an adrenergic receptor agonist), forskolin (an activator of adenylate cyclase), dibutyryl-cAMP (an activator of protein kinase A) and DPCPX (an adenosine A1 receptor antagonist) was diminished in the adipocytes of rats fed an HFD, however, this effect was alleviated by betaine. Moreover, blood leptin levels in HFD-fed rats were elevated, whereas leptinemia have normalized by betaine supplementation. Betaine prevented the increase in expression of N-methyl D-aspartate receptors in the hippocampus and in the cerebral cortex. These results indicate that betaine positively affects the insulin-sensitive tissues: liver (hepatoprotective effects), skeletal muscle (reduced lipid accumulation) and adipose tissue (a rise in lipolysis), which is associated with improved insulin sensitivity. Betaine-induced prevention of hyperleptinemia indicates restoration of leptin action, and changes in the brain reveal neuroprotective properties. Our results show that betaine induces positive changes in HFD-fed rats, its action is pleiotropic and involves different tissues. [ABSTRACT FROM AUTHOR]

Background Resveratrol was found to alleviate consequences of some metabolic disturbances which may be due to inappropriate dietary habits. It decreases mortality, increases insulin sensitivity and improves motor functions; these effects are accompanied by reduced plasma leptin and insulin. Leptin plays a significant role in the regulation of food intake and energy expenditure – elevated level in blood is one of the reasons of leptin-resistance and obesity. In this study, the direct effect of resveratrol on leptin secretion from isolated adipocytes was investigated. Material and methods Isolated rat adipocytes were incubated with resveratrol (62·5, 125 or 250 μM) and its effects on leptin secretion were studied. Cells were incubated with resveratrol in the presence of glucose (5 and 20 mM) and insulin (10 nM); glucose and nicotinic acid (1 mM); glucose and insulin in the presence of an inhibitor of protein kinase A (H-89, 50 μM) or alanine (10 mM) and insulin. The glucose uptake, glycerol release to the incubation medium, lactate and ATP produced by the cells were also measured. Results Resveratrol inhibited leptin secretion in all experimental designs in a dose-dependent manner. The effect was not accompanied by changes in glycerol release and glucose uptake. Adipocyte exposure to resveratrol enhanced the lactate formation. It was found that resveratrol dramatically reduced ATP in adipocytes. Conclusion The obtained results revealed the direct ability of resveratrol to reduce leptin secretion from isolated rat adipocytes. Resveratrol is therefore a compound affecting the endocrine function of adipocytes. [ABSTRACT FROM AUTHOR]

Naringenin is a bioactive flavanone involved in the inhibition of drug metabolism which exhibits antioxidant, anti-inflammatory and anticancerogenic properties and which recently appeared to be a factor mitigating the hyperlipidaemic effects in rats and rabbits. In the performed experiment, the effect of naringenin, administered intragastrically (50 mg/kg) for 2 weeks to normal and ethanol drinking rats, on insulin and leptin levels and on some metabolic parameters was investigated. Naringenin did not change the hormone levels in any group of rats. Blood glucose, triglyceride, total, esterified and free cholesterol and high-density lipoprotein-cholesterol concentrations were also unaffected by this compound. Only free fatty acids were elevated after the naringenin treatment in the water-drinking rats. In spite of unchanged glucose and insulin concentrations in blood, the tested flavanone reduced the glucose/insulin ratio in ethanol-receiving rats. Liver triglycerides, elevated due to ethanol ingestion, were partially normalized by naringenin. Other tested parameters like liver glycogen and cholesterol, muscle triglycerides and glycogen were not altered in any group of rats. The influence of naringenin (62.5, 125, 250 and 500 μm) on basal and insulin-stimulated glucose conversion to lipids (lipogenesis) as well as on basal and epinephrine-stimulated glycerol release (lipolysis) in the isolated rat adipocytes was also tested. The basal and the stimulated lipogenesis tended to be decreased in the presence of the flavanone (250 μm). This inhibitory effect intensified and was statistically significant at the highest concentration of naringenin. The tested compound did not evoke any effect on basal lipolysis while the epinephrine-stimulated process was limited at the highest concentration of the flavanone. Naringenin (62.5, 125, 250 and 500 μm) had no effect on leptin secretion from the isolated rat adipocytes. Results obtained in our studies demonstrate that naringenin exerts a very weak influence on carbohydrate and lipid metabolism of normal and ethanol-consuming rats and on metabolism of isolated rat adipocytes. [ABSTRACT FROM AUTHOR]

Phytic acid (PA) is present in considerable amounts in the seeds of many plant species consumed by animals. Little is known about its influence on metabolic processes. In the performed experiment the effect of rats feeding a standard laboratory diet (Murigran) with increasing supplements of PA on some hormones and biochemical parameters was tested. Male Wistar rats were divided into five groups of eight animals each. In the first group (control) rats were fed a diet without any supplement whereas the groups II–V received food with added PA: 0.1, 0.2, 0.3 and 1%. After 20 days animals were decapitated, blood serum, liver and tight muscles were sampled. In rats fed a diet enriched in PA the concentration of thyroid hormones was diminished. Simultaneously, T3/T4 ratio was slightly reduced. These changes were accompanied by a rise in blood glucose level and an augmentation in liver and muscle glycogen stores and were found in spite of unchanged blood insulin. Consumption of food with increased amounts of PA resulted in a substantial reduction of liver triglyceride content, but serum triglycerides were not affected. In rats from groups II and III serum free-fatty acids concentration was reduced. However, in animals receiving highest PA supplement this effect was not observed. Serum calcium and magnesium were not affected by PA. Serum iron was significantly reduced, but only in rats on the highest supplement of the tested compound. Results obtained in this experiment clearly indicate that the PA is able to induce hormonal and metabolic changes in animals. These changes seem to result not only from reduced bioavailability of minerals but also from interactions of PA with nutrients and enzymes in the liver. [ABSTRACT FROM AUTHOR]

The effect of ethanol drinking on some hormonal and metabolic changes in the rat and on lipolysis in isolated adipocytes was tested. Male growing Wistar rats divided into two groups were used in the experiment. Ten per cent ethanol solution as the only drinking fluid for 2 weeks depressed body weight gain. The diminution of blood insulin with simultaneous increase in leptin concentration found in these rats suggest that the physiological regulation of leptin secretion is disturbed by ethanol. Liver triglycerides content was substantially augmented due to ethanol ingestion. Adipocytes were isolated from both groups of rats by collagenase digestion and the lipolytic activity of these cells was compared. Isolated cells (106/ml) were incubated for 90 min in Krebs–Ringer buffer (pH 7.4, 37 °C) containing 3 m m glucose and different lipolytic modulators: adrenaline (1 μ m), insulin (1 n m), dibutyryl-cAMP (1 m m) and DPCPX (a selective antagonist of adenosine A1 receptor, 1 μ m). To determine basal lipolysis cells were incubated without lipolytic agents. Lipolysis was determined by the amount of glycerol released from cells to the incubation medium. Basal and adrenaline-induced lipolysis was depressed in adipocytes of ethanol-drinking rats. The antilipolytic activity of insulin was the same in both groups of isolated cells. Lipolysis induced by dibutyryl-cAMP was only slightly reduced due to ethanol consumption, whereas triglycerides breakdown evoked by adenosine A1 receptor antagonism was unchanged. Results obtained in vitro indicate that subchronic ethanol drinking attenuates basal and stimulated lipolysis in adipocytes, however, the antilipolytic effect of insulin and the adenosine pathway are unchanged. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Physiology & Biochemistry is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Physiology & Biochemistry is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Changes in thyroid status affect metabolism not only directly, butinfluence it also by alterations in insulin secretion and action. Despiteseveral investigations, these effects are, however, poorly characterised oreven controversial. The aim of the studies was to investigate the effect ofhyperthyreosis (HT) and hypothyreosis (HPT) on insulin binding by rat livermembranes. Some metabolic parameters reflecting insulin and thyroid hormonesaction were also determined. HT and HPT were developed by daily administrationfor 3 weeks of thyroxine (T [sub 4] ) and thiouracil (TU), respectively.Experimental hyperthyreosis and hypothyreosis caused deep changes in metabolism.The greatest alterations were observed in body and thyroid glands weight,blood triiodothyronine (T [sub 3] ), T [sub 4] , glucose, and insulinlevels, liver glycogen amount and number of insulin receptors. HT reflectedin rats in slower rate of growth and in smaller thyroid glands weight. Incomparison to controls, T [sub 4] concentration in HT was almost doubledand it was reduced by about 30% in HPT. Also, T[sub 3] , insulin andglucose levels in HT were heightened. Simultaneously, binding of insulin toliver membranes was elevated in HT and reduced in HPT. In HT the number ofhigh affinity insulin receptors (HAIRs) and low affinity insulin receptors(LAIRs) was increased, whereas in HPT the amount of HAIRs was diminished.HT caused a drastic reduction of glycogen concentration in liver, but no changeswere observed for muscle glycogen. Considering lipid metabolism, only freefatty acids (FFA) level in blood was changed (in HPT), but no differenceswere observed in serum concentration of triglycerides and cholesterol. Severalmetabolic changes observed in HT and HPT seem to be the dire ct consequenceof alterations of thyroid hormone concentrations. These disturbances, togetherwith the direct effect of HT or HPT on insulin secretion, binding and actionlead, in turn, to changes in the other metabolic parameter... [ABSTRACT FROM AUTHOR]

Myo-inositol was found to possess several beneficial effects on theorganism. The effect of myo-inositol on ethanol-induced metabolic changesand insulin concentration was investigated in growing rats. The increase inliver triglycerides induced by ethanol drinking (10% ethanol solution as theonly drinking fluid for 10 days) was completely abolished by simultaneoustreatment with myo-inositol (0.1 g/100 g b.w., every day given intragastrically).The ethanol-evoked decrease in blood insulin and the increase in liver glycogenwere also partially prevented by myo-inositol. Myo-inositol did not causeany undesirable metabolic changes in the rats. The results indicate that myo-inositolmay be useful in the treatment of some metabolic consequences of alcohol drinking. [ABSTRACT FROM AUTHOR]