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41.
Endocannabinoid receptor blockade increases hepatocyte growth factor and reduces insulin levels in obese women with polycystic ovary syndrome 
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Isoflavones, a group of phytoestrogens, are selective oestrogen receptor (ER) modulators. They may positively impact endocrine-related conditions but the current evidence is sparse. Equol, a non-steroidal oestrogen, is produced by the metabolism of the isoflavone daidzein by intestinal bacteria. In Western countries, 30-50% of individuals metabolize daidzein into equol and are known as equol producers. Equol production may be the source of benefit from isoflavones in endocrine disease. 相似文献
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H. Kahal A. Aburima B. Spurgeon K.S. Wraith A.S. Rigby T. Sathyapalan E.S. Kilpatrick K.M. Naseem S.L. Atkin 《Diabetes & metabolism》2018,44(5):431-436
Aim
Strict glycaemic control has been associated with an increased mortality rate in subjects with type 2 diabetes (T2DM). Here we examined platelet function immediately and 24 hours following induced hypoglycaemia in people with type 2 diabetes compared to healthy age-matched controls.Methods
Hyperinsulinaemic clamps reduced blood glucose to 2.8 mmol/L (50 mg/dl) for 1 hour. Sampling at baseline; euglycaemia 5 mmol/L (90 mg/dl); hypoglycaemia; and at 24 post clamp were undertaken. Platelet function was measured by whole blood flow cytometry.Results
10 subjects with T2DM and 8 controls were recruited. Platelets from people with T2DM showed reduced sensitivity to prostacyclin (PGI2, 1 nM) following hypoglycaemia. The ability of PGI2 to inhibit platelet activation was significantly impaired at 24 hours compared to baseline in the T2DM group. Here, inhibition of fibrinogen binding was 29.5% (10.3–43.8) compared to 50.8% (36.8–61.1), (P < 0.05), while inhibition of P-selectin expression was 32% (16.1–47.6) vs. 54.4% (42.5–67.5) (P < 0.05). No significant changes in platelet function were noted in controls.Conclusion
Induced hypoglycaemia in T2DM enhances platelet hyperactivity through impaired sensitivity to prostacyclin at 24 hours. 相似文献44.
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There is a growing body of evidence to suggest that type 2 diabetes is associated with a generalised activation of the innate immune system, in which there is a chronic low-grade inflammation. Further evidence for roles of inflammation in type 2 diabetes comes from clinical studies using either anti-inflammatory approaches or biological agents that target specific proinflammatory cytokine pathways to improve parameters of glucose control especially with IL-1β (Interleukin 1 β) antagonism and salsalate (non-acetylated prodrug of salicylate) treatment. In this review, recent evidence implicating the pathological involvement of the immune system in type 2 diabetes is examined, together with the role of potential treatment modalities targeting the immune system in the management of type 2 diabetes. 相似文献
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