Metabolic syndrome is a cluster including hyperglycaemia, obesity, hypertension, and hypertriglyceridaemia as a result of biochemical and physiological alterations and can increase the risk of cardiovascular disease and diabetes. Fundamental research on this disease requires validated animal models. One potential animal model that is rapidly gaining in popularity is zebrafish (Danio rerio). The use of zebrafish as an animal model conveys several advantages, including high human genetic homology, transparent embryos and larvae that allow easier visualization. This review discusses how zebrafish models contribute to the development of metabolic syndrome studies. Different diseases in the cluster of metabolic syndrome, such as hyperglycaemia, obesity, diabetes, and hypertriglyceridaemia, have been successfully studied using zebrafish; and the model is promising for hypertension and cardiovascular metabolic-related diseases due to its genetic similarity to mammals. Genetic mutation, chemical induction, and dietary alteration are among the tools used to improve zebrafish models. This field is expanding, and thus, more effective and efficient techniques are currently developed to fulfil the increasing demand for thorough investigations.
Surgery induces a 'stress' state leading to post-operative hyperglycaemia. To investigate this effect on patients with Type 2 Diabetes Mellitus, we reviewed the records of 50 diabetic patients who underwent surgery without intraoperative insulin. Demographic features together with pre-operative and post-operative blood glucose readings were noted. 27.3% of patients with well controlled pre-operative blood glucose levels developed post-operative hyperglycaemia. In contrast, 84.6% of patients with poorly controlled levels developed the same. Poor control of blood glucose and duration of operation were the only significant predictors of post-operative hyperglycaemia.
We investigated if vitamin D is independently associated with hyperglycaemia in gestational diabetes mellitus (GDM). Serum 25 hydroxy vitamin D (25OHD), fasting blood glucose (FBG), HbA1c, fructosamine, insulin sensitivity (QUICKI equation), body mass index, clothing style and outdoor activity were measured in 58 pregnant women with GDM during the third trimester. 25OHD was also measured in 20 women with normal pregnancies. There was no significant difference in mean 25OHD concentrations between GDM (14.43 ± 5.27 ng/ml) and normal (15.45 ± 5.29 ng/ml) pregnancies, p = .354. However, a higher percentage of GDM subjects had 25OHD concentration <19.8 ng/ml (86 versus 65%, p = .003). 25OHD did not correlate with FBG, HbA1c, fructosamine, insulin sensitivity or insulin dosage (p > .05). On multivariate analysis, only ethnicity (p = .006) and outdoor activity (p = .004) were associated with 25OHD. We conclude that the lower 25OHD levels in our GDM patients were related to ethnicity and outdoor activity (Study FF-2017-111, National University of Malaysia, 16 March 2017).IMPACT STATEMENTWhat is already known on this subject? Vitamin D deficiency in pregnancy is widespread and particularly in certain ethnic groups. Low vitamin D levels may be an aetiological factor for gestational diabetes mellitus (GDM) but previous studies provide conflicting results perhaps due to confounding factors.What do the results of this study add? In this study of pregnant women with GDM from different ethnic backgrounds, we analysed serum 25-hydroxy vitamin D (25OHD) levels together with other confounding factors, that is, body mass index, ethnicity and sunlight exposure. Furthermore, instead of using consensus values, we determined cut-offs for different vitamin D status from normal pregnancies matched for gestational age and ethnicity. We found that a higher percentage of GDM subjects had lower vitamin D status but there was no correlation with hyperglycaemia or insulin sensitivity. The study showed that lower vitamin D levels in GDM was associated with ethnicity and less outdoor activity.What the implications are of these findings for clinical practice and/or further research? In GDM patients, low vitamin D levels may be modifiable by supplementation or lifestyle change. Longitudinal studies are needed to determine whether this would impact on the occurrence of GDM.
The present study explored the hypothesis that a prolonged 8 weeks exposure to a high fructose intake suppresses adrenergic and angiotensin II (Ang II)-mediated vasoconstriction and is associated with a higher contribution of α1D-adrenoceptors. A total of thirty-two Sprague-Dawley rats received either 20 % fructose solution (FFR) or tap water (control, C) to drink ad libitum for 8 weeks. Metabolic and haemodynamic parameters were assessed weekly. The renal cortical vasoconstrictor responses to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II were determined in the presence and absence of BMY7378 (α1D-adrenoceptor antagonist). FFR had increased blood pressure, plasma levels of glucose, TAG and insulin. FFR expressed reduced renal vascular responses to adrenergic agonists and Ang II (NA: 50 %, PE: 50 %, ME, 65 %, Ang II: 54 %). Furthermore in the C group, the magnitude of the renal cortical vasoconstriction to all agonists was blunted in the presence of the low or high dose of BMY7378 (NA: 30 and 31 %, PE: 23 and 33 %, ME: 19 and 44 %, Ang II: 53 and 77 %), respectively, while in the FFR, vasoconstriction was enhanced to adrenergic agonists and reduced to Ang II (NA: 8 and 83 %, PE: 55 %, ME, 2 and 177 %, Ang II: 61 and 31 %). Chronic high fructose intake blunts vascular sensitivity to adrenergic agonists and Ang II. Moreover, blocking of the α1D-adrenoceptor subtype results in enhancement of renal vasoconstriction to adrenergic agonists, suggesting an inhibitory action of α1D-adrenoceptors in the FFR. α1D-Adrenoceptors buffer the AT1-receptor response in the renal vasculature of normal rats and fructose feeding suppressed this interaction.
The aims of the present study were to assess the control of glycemia and other cardiovascular disease risk factors, and the association between age and these controls among older adults with type 2 diabetes in Malaysia.
PURPOSE: Fructose feeding induces a moderate increase in blood pressure, insulin resistance, and hyperinsulinemia. This study investigated the role of α(1B)-adrenoceptor subtype in the control of renal hemodynamic responses to exogenously administered angiotensin II (Ang II) and a set of adrenergic agonists in a model of high fructose-fed rats.
METHODS: Sprague-Dawley rats were fed for 8 weeks with 20% fructose in drinking water (FFR). The renal cortical vasoconstriction to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II in the presence and absence of chloroethylclonidine (CEC) (α(1B)-adrenoceptor antagonist) was determined. Data, mean ± SEM or SD were subjected to ANOVA with significance at p