Dynamic retinal vessel response to flicker in obesity: A methodological approach

Kotliar, Konstantin; Lanzl, Ines; Schmidt‐Trucksäss, Arno; Sitnikova, D.; Ali, Mohammad; Blume, K. G.; Halle, Martin; Hanssen, Henner

doi:10.1016/j.mvr.2010.11.007

Cited by 71 publications

(78 citation statements)

References 25 publications

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“…These differences were independent of major confounders such as BMI, mean arterial pressure and sex. Baseline insulin status was independently The retinal microcirculation is well suited for studying the association between insulin resistance and vascular function as it has been shown to be compromised over a wide hyperglycaemic continuum, thereby possibly contributing to the development of diabetic retinopathy and vision loss [5,7,14]. Against previous evidence in healthy obese [14] and individuals with moderately elevated HbA 1c [7], our results indicate that the hyperaemic flicker response of retinal arteries is not reduced but heightened in early insulin resistance.…”

Section: Discussionmentioning

confidence: 46%

“…Baseline insulin status was independently The retinal microcirculation is well suited for studying the association between insulin resistance and vascular function as it has been shown to be compromised over a wide hyperglycaemic continuum, thereby possibly contributing to the development of diabetic retinopathy and vision loss [5,7,14]. Against previous evidence in healthy obese [14] and individuals with moderately elevated HbA 1c [7], our results indicate that the hyperaemic flicker response of retinal arteries is not reduced but heightened in early insulin resistance. It appears that previous findings were either not adjusted for differences in mean arterial pressure or were confounded by concomitant intake of statins and antihypertensive drugs, which are known to influence retinal diameters and flicker responses [16,17].…”

Section: Discussionmentioning

confidence: 46%

“…It has been suggested that increases in blood flow and inflammation associated with hyperglycaemia and retinal hypoxia may be primarily responsible for changes in retinal venous function and thus may subsequently develop with the onset of chronic dysglycaemic conditions [37]. However, a previous study also demonstrated reduced retinal venous responses to flicker-light in obesity, although the study did not control for significantly higher glucose levels in the obese individuals [14]. In our study, insulin-sensitive and insulin-resistant individuals had comparable fasting glucose levels, which may additionally explain undisturbed retinal venous flicker responses.…”

Section: Discussionmentioning

confidence: 86%

“…The peak-to-peak value was manually calculated as the difference between the maximal and minimal arterial diameters. The area under the reaction curve during flicker stimulation was calculated in [%×s] as described previously by Kotliar et al [14]. The purpose was to assess differences in the curve form during flicker stimulation.…”

Section: Assessment Of Glucose Tolerance and Insulin Sensitivitymentioning

confidence: 99%

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Insulin is a key determinant of elevated retinal arteriolar flicker response in insulin-resistant individuals

Reimann

Vilser²,

Grüber

et al. 2015

Diabetologia

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Aims/hypothesis Insulin may link metabolic disorders to retinal microvascular pathology. The aim of the present study was to investigate the impact of early insulin resistance on retinal microcirculation. Methods Retinal diameter responses to flicker-light stimulation were investigated in 81 clinically healthy participants (32 ±6 years [mean±SD], 59% women) who were recruited according to their BMI. All participants underwent an OGTT and euglycaemic-hyperinsulinaemic clamp (40 mU/m 2 · min −1 insulin dose). After stratification by low and high insulin sensitivity based on a clamp-derived glucose disposal rate of ≤ or >4.9 mg/kg body mass, respectively, baseline retinal diameters and their relative changes to flicker stimulation were compared while controlling for mean arterial pressure, BMI and sex.Results The arterial vasodilator response at the end of flicker stimulation (p=0.044) and the area under the arterial reaction curve during flicker stimulation (p=0.015) were significantly higher in individuals with low vs high insulin sensitivity. Vasodilatory responses of retinal veins to flicker stimulation and baseline retinal diameters did not differ between insulinsensitive and insulin-resistant participants (p>0.05). In a stepwise linear regression analysis, fasting insulin remained the only predictor of the arterial vasodilator response to flicker-light (p<0.01). Waist circumference also contributed, although to a lesser extent, to the arterial vasodilator response (p=0.023). Conclusions/interpretation Insulin sensitivity is an important determinant of retinal microvascular function. We propose that the elevated arterial flicker response in insulin-resistant states is a result of higher circulating insulin levels.

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Section: Discussionmentioning

confidence: 46%

Section: Discussionmentioning

confidence: 46%

Section: Discussionmentioning

confidence: 86%

Section: Assessment Of Glucose Tolerance and Insulin Sensitivitymentioning

confidence: 99%

See 2 more Smart Citations

Insulin is a key determinant of elevated retinal arteriolar flicker response in insulin-resistant individuals

Reimann

Vilser²,

Grüber

et al. 2015

Diabetologia

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“…Additionally baseline diameter fluctuation (peakto-trough amplitude prior to flicker onset), dilation amplitude (difference between maximum and minimum dilation), and time to reach maximum dilation can also be assessed and this set of five parameters is sometimes termed sequential diameter response analysis (SDRA) 16 ; though note other forms of analysis have been attempted. 9,17,18 The aim of this study was firstly to evaluate how FL duration affected the various SDRA parameters; for example, how is maximum dilation/ maximum constriction affected by flicker duration? The second goal was to evaluate individual flicker cycles and assess the variability in SDRA parameters across flicker cycles in protocols of different FL duration.…”

mentioning

confidence: 99%

The Time Course of Changes in Retinal Vessel Diameter in Response to Differing Durations of Flicker Light Provocation

Heitmar

Summers

2015

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To determine the response of retinal vessels to differing durations of flicker light (FL) stimulation. METHODS.We recorded retinal arterial and venous vessel dilation to 12.5 Hz FL provocation of varying duration (5, 7, 10, and 20 seconds) in 12 healthy young individuals (age range, 26-45 years). All participants underwent a full ocular examination including IOP and blood pressure measurements.RESULTS. Maximum dilation (MD) did not show a significant dependence on flicker duration in arteries, whereas maximum constriction (MC) did. In veins, however, MD significantly increased with flicker duration. Approximately 80% to 90% of MD in arteries is reached within 10 seconds of FL stimulation.CONCLUSIONS. The vast majority of arterial dilatory capacity is reached within 10 seconds of FL stimulation even though venous dilation continues strongly. Since MC of arteries shows a significant dependence on flicker duration, measurements at two different durations can provide more information about the retinal vascular system than at a single flicker duration alone.

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Developmental Conditioning of the Vasculature

Clough

2014

Comprehensive Physiology

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There is increasing evidence from epidemiological and experimental animal studies that the early life environment, of which nutrition is a key component, acts through developmental adaptive responses to set the capacity of cardiovascular and metabolic pathways to respond to physiological and pathophysiological challenges in later life. One finding that is consistent to both population studies and animal models is the propensity for such effects to induce endothelial dysfunction throughout the vascular tree, including the microvasculature. Obesity, type 2 diabetes and hypertension are associated with changes in microvascular function affecting multiple tissues and organs. These changes may be detected early, often before the onset of macrovascular disease and the development of end organ damage. Suboptimal maternal nutrition and fetal growth result in reduced microvascular perfusion and functional dilator capacity in the offspring, which together with microvascular rarefaction and remodeling serve to limit capillary recruitment, reduce exchange capacity and increase diffusion distances of metabolic substrates; they also increase local and overall peripheral resistance. This article explores how a developmentally conditioned disadvantageous microvascular phenotype may represent an important and additional risk factor for increased susceptibility to the development of cardio-metabolic disease in adult life and considers the cell signaling pathways associated with microvascular dysfunction that may be "primed" by the maternal environment. As the microvasculature has been shown to be a potential target for early therapeutic and lifestyle intervention, this article also considers evidence for the efficacy of such strategies in humans and in animal models of the developmental origins of health and disease.

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Dynamic retinal vessel response to flicker in obesity: A methodological approach

Cited by 71 publications

References 25 publications

Insulin is a key determinant of elevated retinal arteriolar flicker response in insulin-resistant individuals

Insulin is a key determinant of elevated retinal arteriolar flicker response in insulin-resistant individuals

The Time Course of Changes in Retinal Vessel Diameter in Response to Differing Durations of Flicker Light Provocation

Developmental Conditioning of the Vasculature

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