The aim of the study was to analyze the thickness of individual retinal layers in patients with type 1 diabetes (T1D) in comparison to the control group and in relation to markers of diabetes metabolic control. The study group consisted of 111 patients with an average of 6-years of T1D duration. The control group included 36 gender- and age-matched individuals. In all patients optical coherence tomography (OCT) study was performed using HD-OCT Cirrus 5000 with evaluation of optic nerve head (ONH) parameters, thickness of retinal nerve fiber layer (RNFL) with its quadrants, macular full-thickness parameters, ganglion cells with inner plexus layer (GCIPL) and choroidal thickness (CT). Lower disc area value was observed in the study group as compared to controls (p = 0.0215). Negative correlations were found both between age at examination and rim area (R = −0.28, p = 0.0007) and between superior RNFL thickness and duration of diabetes (R = −0.20, p = 0.0336). Positive correlation between center thickness and SD for average glycemia (R = 0.30, p = 0.0071) was noted. Temporal CT correlated positively with age at examination (R = 0.21, p = 0.0127). The selected parameters the HD-OCT study may in the future serve as potential markers of preclinical phase of DR in patients with T1D.
TBC1D1 and TBC1D4 proteins play analogous, but not identical role in governing insulin-signalling pathway. Little is known about changes in expression levels of
TBC1D1
and
TBC1D4
genes in mammals, including humans. Number of factors were studied, but data remain controversial. The aim of this study was to evaluate the effect of selected cytokines, adipokines and myokines with known or putative insulin sensitivity regulation activity (adiponectin, irisin, omentin, interleukin 6, leptin, resistin, and tumour necrosis factor) on
TBC1D1
and
TBC1D4
expression levels in cultured differentiated human adipocytes. No significant differences were found between the adipocytes treated with different stimuli and this effect was determined not dose dependent. It is reasonable to conclude that relative shortage of data showing no change in TBC1D1 and TBC1D4 from literature results from publication bias; therefore, our finding provides additional insight into the role of both genes.
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