Diabetic retinopathy (DR) is the most common microvascular complication of diabetes mellitus, leading to visual impairment if left untreated. This review discusses the use of optical coherence tomography angiography (OCTA) as a diagnostic tool for the early detection and management of DR. OCTA is a fast, non-invasive, non-contact test that enables the detailed visualisation of the macular microvasculature in different plexuses. OCTA offers several advantages over fundus fluorescein angiography (FFA), notably offering quantitative data. OCTA is not without limitations, including the requirement for careful interpretation of artefacts and the limited region of interest that can be captured currently. We explore how OCTA has been instrumental in detecting early microvascular changes that precede clinical signs of DR. We also discuss the application of OCTA in the diagnosis and management of various stages of DR, including non-proliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), diabetic macular oedema (DMO), diabetic macular ischaemia (DMI), and pre-diabetes. Finally, we discuss the future role of OCTA and how it may be used to enhance the clinical outcomes of DR.

BACKGROUND: In recent years, the role of vaspin as an insulin-sensitizer has been studied widely. This is the investigation that examined the association of vaspin polymorphism rs2236242 on the vaspin level and the risk of type 2 diabetes and insulin-resistant Iranian pre-diabetic/diabetic population.
METHODS: A case-control study was conducted on 160 participants includes 80 participants holding (FBG) fasting blood glucose 3.88-5.55 (mmol/L) in the normal group, and 80 participants holding FBG≥5.55 (mmol/L) in a diabetic/pre-diabetic group. The serum vaspin and insulin were determined with ELISA (enzyme-linked assay) and biochemical variables by standard method. Tetra arms amplification system for the vaspin gene was performed. Statistical analysis was done using SPSS software version 20.
RESULTS: The means of age, body mass index (BMI), waist circumference (WC), hip circumference (HC), FBG, and vaspin were significantly different between normal and type 2 diabetic/impaired fasting blood group (P-value<0.05). rs2236242 showed association with Hip circumference (P-value<0.05). A significant association between allele A of rs2236242 with type 2 diabetes was seen (P-value<0.001). The vaspin levels showed a negative correlation with FBG (r =-0.296, P=0.001).
CONCLUSIONS: Allele A of rs2236242 is a protective risk for type 2 diabetes, but no association of rs2236242 with insulin resistance was seen. The lower level of vaspin is a predictor for the progression of type 2 diabetes.
UNASSIGNED: Poslednjih godina dosta je proučavana uloga vaspina kao senzitizatora insulina. Ovo istraživanje je proučavalo povezanost polimorfizma vaspina rs2236242 na nivou vaspina i rizik od dijabetesa tipa 2 kod iranske populacije predijabetičara i dijabetičara rezistentne na insulin.
METHODS: Sprovedena studija je uključivala 160 učesnika. Kod 80 učesnika nivo glukoze u krvi je bio 3,88-5,55 mmol/L - kontrolna grupa koja nije uzimala hranu pre davanja uzoraka (FBG), i 80 učesnika kod kojih je nivo FBG bio ≥ 5,55 mmol/L - grupa dijabetičara / predijabetičara). Serumski vaspin i insulin određeni su ELISA testom i biohemijskim varijablama standardnom metodom. Primenjen je tetra arms sistem za pojačavanje gena vaspina. Statistička analiza je urađena uz pomoć softvera SPSS, verzija 20.
UNASSIGNED: Srednje vrednosti životne dobi, indeksa telesne mase (BMI), obima struka (WC), obima kuka (HC), FBG i vaspina su se značajno razlikovale između kontrolne grupe sa normalnim vrednostima i vrednosti u grupi dijabetičara tipa 2 (P vrednost < 0,05). rs2236242 je pokazao povezanost s obimom kuka (P-vrednost < 0,05). Primećena je značajna povezanost alela A rs2236242 sa dijabetesom tipa 2 (P-vrednost < 0,001). Nivoi vaspina pokazali su negativnu korelaciju sa FBG-om (r = -0,296, P = 0,001).
UNASSIGNED: Alel A rs2236242 je zaštitni rizik za dijabetes tipa 2, ali nije primećena povezanost rs2236242 sa rezistencijom na insulin. Niži nivo vaspina je prediktor za progresiju dijabetesa tipa 2.

Alzheimer\'s disease (AD) is a progressive neurodegenerative disease characterized by beta-amyloid (Aβ) deposition, neurofibrillary tangles and cognitive decline. Clinical data suggests that both type 1 and type 2 diabetes are risk factors for AD-related dementia and several clinical studies have demonstrated that AD patients show alterations in peripheral glucose regulation characterized by insulin resistance (hyperinsulinemia) or hypoinsulinemia. Whether animal models of AD exhibit a pre-diabetic phenotype without additional dietary or experimental manipulation is unclear however, with contradictory data available. Further, most studies have not examined the time course of potential pre-diabetic changes relative to AD pathogenesis and cognitive decline. Thus, in this study we tested the hypothesis that a pre-diabetic phenotype (peripheral metabolic dysregulation) exists in the APP/PS1 transgenic model of AD under normal conditions and precedes AD-related pathology. Specifically, we examined glucose tolerance in male APP/PS1 mice on a C57BL/6J congenic background at 2, 4-6 and 8-9months of age by assessing fasting glucose levels, glucose tolerance, plasma insulin levels and insulin sensitivity as well as the development of pathological characteristics of AD and verified that our APP/PS1 mice develop cognitive impairment. Here we show that APP/PS1 mice, compared to wild-type controls, exhibit a significant impairment in glucose tolerance during an intraperitoneal glucose tolerance test (ipGTT) and a trend for increased fasting plasma insulin concentrations as early as 2months of age, while extracellular Aβ1-42 deposition occurs later and cognitive decline exists at 8-9months of age. Moreover, APP/PS1 mice did not respond as well to exogenous insulin as the wild-type controls during an intraperitoneal insulin tolerance test (ipITT). Taken together, these data reveal that male APP/PS1 mice on a C57BL/6J congenic background exhibit a pre-diabetic phenotype prior to the development of AD-like pathology and that this metabolic deficit persists when they exhibit neuropathology and cognitive decline. This raises the question of whether altered glucose regulation and insulin production/secretion could contribute to AD pathogenesis.

BACKGROUND: Chromium supplementations (Cr) have been shown to exert beneficial effects in the management of type-2 diabetes. Prevalence of Cr deficiency in pre-diabetic patients is not well-understood, therefore, the aim of this study was to evaluate the extent of this prevalence.
METHODS: In this cross-sectional descriptive study, 132 pre-diabetic patients were recruited. The participants were randomly selected from those who referred to the Shariati Hospital in Isfahan, Iran. Blood samples are collected for measurement of Cr, insulin, fasting blood sugar (FBS), and two-hour post-load plasma glucose. The body mass index (BMI) was calculated. Determination of Cr was carried out by atomic absorption spectrometry.
RESULTS: Thirty-four (31.5%) patients had Cr deficiency and 74 (68.5%) patients had normal Cr. There was no significant difference between sex, age groups (<50 years and ≥50 years) and between patients with and without a family history of diabetes in both the groups. No significant differences in age, BMI, FBS or insulin were observed between two groups. In the group with a normal level of Cr, there was a significant reversed correlation between the Cr level and age, but no significant correlation existed between the Cr level and other factors in both groups.
CONCLUSIONS: The levels of Cr deficiency are relatively common in patients with pre-diabetes, and it is necessary to screen patients with diabetes and pre-diabetes according to the American Diabetes Association guidelines, with regard to the Cr level and action should be taken to eliminate the Cr deficiency in these patients.

BACKGROUND: Chronic or severe acute elevations in plasma glucose are associated with decreases in the number and function of circulating angiogenic cells (CACs). However, less is known about whether fasting plasma glucose levels (FPG) within the normal or pre-diabetic range among healthy individuals are associated with decreased CAC function. Establishing this relationship is an important step in developing a line of research that may ultimately lead to preventative lifestyle interventions intended to maximize endogenous CAC function and reduce cardiometabolic disease risk.
OBJECTIVE: 1) To examine whether increases in FPG are associated with decreases in CAC migration among healthy individuals with FPG levels below the threshold for hyperglycemia, and 2) to contrast effect of FPG on CAC migration toward a pro-angiogenic stimulus (vascular endothelial growth factor; VEGF) with effect on intrinsic cell migratory capacity (i.e., random migration with no stimulus).
METHODS: 28 men and women ranging from 20-57 years of age and free of cardiovascular disease participated in a pilot study, involving a fasting blood draw for FPG and isolation of peripheral blood mononuclear cells. CAC migration toward VEGF and random cell migration (control) were assessed in vitro. VEGF-induced migration that was normalized to control migration, representing the VEGF-response component of chemotaxis independent of motility, was calculated to determine whether any impairment in migration to VEGF was due to lower specific response to VEGF or to lower non-specific migratory capacity.
RESULTS: Increased levels of FPG were associated in a dose-response fashion with a significantly lower random migration under control conditions (CTRL: r= -.408, p=.031), no differences in migration to VEGF (r= -.039, p=.842) and a borderline association with VEGF-induced migration normalized to control migration (VEGF/CTRL: r=.349, p=.069). The relationship between FPG and random migration under control conditions remained significant when controlling for gender and body mass index (p\'s<.05), and became borderline significant when controlling for age (p=.062).
CONCLUSIONS: Among healthy individuals, higher fasting glucose levels, despite falling below the diabetic range, are associated with decreased random CAC migration. These findings suggest a need for further studies investigating the effects of lifestyle or dietary interventions on glucose regulation and CAC function.