Contents
01.12.2021.
Professional paper
Fructose metabolism: The pathogenic potential of a little molecule
In recent decades, the use of fructose in diet has increased worldwide, and coincided with increase of obesity, metabolic syndrome, diabetes, and non-alcoholic liver disease. This review presents molecular aspects of fructose metabolism, its characteristics and contemporary knowledge about control mechanisms in order to answer how this small molecule can exert pathogenic effects. When present in small, physiological amounts, fructose actually exerts protective glycoregulatory effects. However, long-term exposure to supraphysiological amounts of fructose creates conditions for the development of certain pathological states. In such conditions, lipogenesis is intensified causing dyslipidemia, gluconeogenesis is also intensified leading to hyperglycemia and compensatory hyperinsulinemia, while insulin signaling through IP3K/Akt is blocked. Moreover, exposure to high fructose levels can induce inflammation, redox balance disruption and a decline in energy synthesis. It is most likely that the ability of the liver to metabolize large amounts of fructose and the absence of autoregulatory and hormonal control mechanisms are responsible for pathogenic potential of fructose.
Dijana Mirić, Bojana Kisić, Dragana Pavlović, Ilija Dragojević, Sladoje Puhalo
01.12.2019.
Professional paper
Relationship between ACR and other determinants of microalbuminuria in T2DM patients
Introduction: The occurrence of microalbuminuria in type 2 diabetes mellitus (T2DM) patients is regarded as an early clinical sign of incipient kidney damage. Microalbuminuria is often evaluated as urinary albumin to urinary creatinine ratio (ACR). Aim: To assess determinants of microalbuminuria in T2DM patients without prior diagnosis of nephropathy using ACR cut-off values. Materials and Methods: ACR was measured in a total of 90 T2DM patients, during two months in three non-consecutive days, and routine biochemical analyses were performed, including glycated hemoglobin (HbA1c), serum uric acid (SUA), and atherogenic index of plasma (AIP). The cut-off values of ACR were ≤ 2.5 mg/mmol in males, and ≤ 3.5 mg/mmol in females. Duration of T2DM, history of hypertension, HbA1c, estimated glomerular filtration rate (eGFR), AIP, and SUA were investigated for association with microalbuminuria. Results: According to ACR patients were considered as non-albuminuric (n= 57) and microalbuminuric (n = 33). Compared to non-albuminuric group, microalbuminuric group had increased urinary creatinine, urinary albumin, HbA1c, triglycerides and SUA, whilst decreased HDL-cholesterol levels. Although eGFR was generally reduced, the correlation between LogACR and eGFR was not significant (p > 0.05). However, the correlation between LogACR and LogHbA1c was significant. The multiple logistic regression analysis revealed HbA1c (t = 3.42; p = 0.012) and SUA (t = 2.44; p = 0.040) as independent predictors of microalbuminuria in T2DM patients. Conclusion: At ACR cut-off values, concentrations of HbA1c and SUA were independent predictors of microalbuminuria in T2DM patients not yet diagnosed with nephropathy.
Dijana Mirić, Bojana Kisić, Dragana Puhalo-Sladoje, Bratislav Mirić, Dragiša Rašić, Ilija Dragojević, Dragana Pavlović
