Effect of omega-3 fatty acids on glucose homeostasis: role of free fatty acid receptor 1

El-Fayoumi, Shaimaa H.; Mahmoud, A. A.; Fahmy, Aly A.; Ibrahim, Islam A.A.E.-H.

doi:10.1007/s00210-020-01883-5

Cited by 13 publications

(11 citation statements)

References 58 publications

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“…Very low β-arrestin2 levels are associated with the development of IR [9]. In harmony with our previous studies [13, 14], the current study showed that HFrHFD-induced IR was associated with severe downregulation of β-arrestin2 in the classical insulin target tissues like adipose tissue, liver, and skeletal muscle.…”

Section: Discussionsupporting

confidence: 90%

“…Supporting our interpretation, a previous study showed that pioglitazone can acutely inhibit insulin secretion independent of its insulin-sensitizing effect [30]. Also, we showed previously that eicosapentanoic acid, an FFAR1/4 agonist, can enhance insulin sensitivity and reduce insulin secretion independently leading to slight hyperglycemia [13].…”

Section: Discussionsupporting

confidence: 87%

“…We showed previously and in the current study that feeding Swiss albino mice with HFrHFD for 16 weeks induces an early stage of IR characterized by slightly reduced or normal body weight, normo- or slight hyperglycemia, and profound hyperinsulinemia [13, 14]. Both fructose and saturated fats used in this type of diet contribute to the IR state by promoting the degradation of the IRS-1 and downregulation of the insulin receptors [21, 22].…”

Section: Discussionmentioning

confidence: 86%

“…All the procedures were performed according to the manufacturers’ instructions. ELISA technique for measuring β-arrestin2, PIP2, DAG, and phosphoserine 473 of Akt has been previously described [13, 14, 20].…”

Section: Methodsmentioning

confidence: 99%

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Pioglitazone Enhances β-Arrestin2 Signaling and Ameliorates Insulin Resistance in Classical Insulin Target Tissues

et al. 2021

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Introduction: Pioglitazone is a thiazolidinedione oral antidiabetic agent. This study aimed to investigate the effects of pioglitazone as insulin sensitizer on β-arrestin2 signaling in classical insulin target tissues. Methods: Experiments involved three groups of mice; the first one involved mice fed standard chow diet for 16 weeks; the second one involved mice fed high-fructose, high-fat diet (HFrHFD) for 16 weeks; and the third one involved mice fed HFrHFD for 16 weeks and received pioglitazone (30 mg/kg/day, orally) in the last four weeks of feeding HFrHFD. Results: The results showed significant improvement in the insulin sensitivity of pioglitazone-treated mice as manifested by significant reduction in the insulin resistance index. This improvement in insulin sensitivity was associated with significant increases in the β-arrestin2 levels in the adipose tissue, liver, and skeletal muscle. Moreover, pioglitazone significantly increased β-arrestin2 signaling in all the examined tissues as estimated from significant increases in phosphatidylinositol 4,5 bisphosphate and phosphorylation of Akt at serine 473 and significant decrease in diacylglycerol level. Conclusion: To the best of our knowledge, our work reports a new mechanism of action for pioglitazone through which it can enhance the insulin sensitivity. Pioglitazone increases β-arrestin2 signaling in the adipose tissue, liver, and skeletal muscle of HFrHFD-fed mice.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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Pioglitazone Enhances β-Arrestin2 Signaling and Ameliorates Insulin Resistance in Classical Insulin Target Tissues

et al. 2021

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“…For example, omega-3 polyunsaturated fatty acid intake modulated postprandial glucose metabolism in obese mice through a glucagon-like peptide-1 (GLP-1)based pathway [25]. EPA treatment increased blood glucose levels after glucose loading in controlled low-fat-diet-fed mice, but improved glucose tolerance in high-fructose/high-fat-diet-fed mice [26]. These observations imply the possibility that selective consumption of omega-3 polyunsaturated fatty-acid-rich fish oil at the end of the day helps the regulation of glucose metabolism on high-fat-diet-induced obesity, but would have a less marked effect under normal conditions.…”

Section: Discussionmentioning

confidence: 99%

Selective Consumption of Fish Oil at End of the Day Increases the Physiological Fatty Acid Compositions of Eicosapentaenoic Acid and Docosahexaenoic Acid in Mice

et al. 2022

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Diets with high daily fat consumption are associated with excess weight. However, the effects of fat type and consumption timing on excess weight remain unclear. We investigated the selection of a 30% (w/w) fat diet of soybean oil (SOY), lard (LARD), and fish oil (FISH) on the metabolic parameters of mice. Male C57BL/6 mice were divided into the double SOY-box (w-SOY), SOY-box/LARD-box (SOY-vs-LARD), or SOY-box/FISH-box (SOY-vs-FISH) groups and allowed to selectively consume for 8 weeks. The total energy intake was similar for all groups, but the mice selectively chose to consume LARD over SOY and SOY over FISH. Body weight in the SOY-vs-LARD group was significantly higher than that in the w-SOY and SOY-vs-FISH groups. Additionally, minimal but selective consumption of an omega-3 fatty-acid-rich FISH diet at the end of the active period increased the physiological fatty acid compositions of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the SOY-vs-FISH group; their metabolic parameters were also lower than the SOY-vs-LARD group. In conclusion, selectively consuming small amounts of fish oil at the end of the day may prevent excess weight compared with LARD consumption.

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Carvedilol ameliorates dexamethasone-induced myocardial injury in rats independent of its action on the α1-adrenergic receptor

Mohamed

Ahmad

Omran

et al. 2022

Naunyn-Schmiedeberg's Arch Pharmacol

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The current study aimed to investigate the cardiotoxic effect of dexamethasone-high-dose in rats, the therapeutic effect of carvedilol and the role of α1-adrenergic receptor (α1AR). The experiment involved 6 groups: control, dexamethasone (10 mg/kg), carvedilol (10 mg/kg), phenylephrine (1 mg/kg), phenylephrine plus carvedilol and propranolol (30 mg/kg). Drugs and vehicles were given for 7 days. Dexamethasone was given with the drugs in the last 4 groups. On the 8th-day and after overnight fasting, serum and cardiac samples were collected. Serum levels of cardiac troponin I and creatine kinase–myoglobin as well as cardiac levels of diacylglycerol, malondialdehyde, kinase activity of Akt, transforming growth factor-β, Smad3 and alpha smooth muscle actin were measured. Cardiac samples were also used for histopathological examination using hematoxylin–eosin and Sirius red stains, in addition to immunohistochemical examination using β-arrestin2 antibody. Dexamethasone induced cardiac injury via increasing oxidative stress, apoptosis and profibrotic signals. Carvedilol significantly reduced the dexamethasone-induced cardiotoxicity. Using phenylephrine, a competitive α1-agonist, with carvedilol potentiated the cardioprotective actions of carvedilol. Propranolol, a β-blocker without activity on α1ARs, showed higher cardiac protection than carvedilol. Dexamethasone-high-dose upregulates cardiac oxidative stress, apoptotic and profibrotic signals and induces cardiac injury. Blocking the α1-adrenergic receptor by carvedilol attenuates its cardioprotective effects against dexamethasone-induced cardiotoxicity.

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Effect of omega-3 fatty acids on glucose homeostasis: role of free fatty acid receptor 1

Cited by 13 publications

References 58 publications

Pioglitazone Enhances β-Arrestin2 Signaling and Ameliorates Insulin Resistance in Classical Insulin Target Tissues

Pioglitazone Enhances β-Arrestin2 Signaling and Ameliorates Insulin Resistance in Classical Insulin Target Tissues

Selective Consumption of Fish Oil at End of the Day Increases the Physiological Fatty Acid Compositions of Eicosapentaenoic Acid and Docosahexaenoic Acid in Mice

Carvedilol ameliorates dexamethasone-induced myocardial injury in rats independent of its action on the α1-adrenergic receptor

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