Introduction: It is well established that microvascular structures are affected in obese people with metabolic disease. We aimed to evaluate the effect on microvascular structures by examining macular and peripapillary vessel density with optical coherence tomography angiography after bariatric surgery in obese individuals without metabolic disease. Methods: This prospective study included 96 eyes of 48 obese patients. Body mass index (BMI), macular vessel density in the superficial, intermediate, and deep capillary plexus, and peripapillary vessel density were measured before and 6 months after bariatric surgery. Results: BMI decreased significantly to 43.75 ± 4.4 kg/m2 postoperatively compared to 55.31 ± 5.1 kg/m2 preoperatively (p < 0.05). A significant increase was observed in macular vessel density in the deep capillary plexus postoperatively (p < 0.01). However, no significant postoperative increase occurred in macular vascular density in the superficial and intermediate capillary plexus (p > 0.05). Moreover, there was no change in peripapillary vascular density (p > 0.05). Postoperative thickening of the foveal, parafoveal, and perifoveal retinal layers was significant (p < 0.001). No significant correlation was detected between BMI change and macular and peripapillary vessel density changes (p > 0.05). Conclusion: An increase in macular vascular density, particularly in the deep capillary plexus, and retinal layer thickness has been observed following bariatric surgery performed on obese individuals without metabolic disease. This increase may indicate that microvascular structures are affected even in the absence of metabolic disease and that microperfusion improves with surgery.

Today, obesity is a major public health problem. The prevalence of this problem is increasing day by day with the diseases and deaths it causes [1]. Particularly, metabolic diseases such as cardiovascular diseases, diabetes, hypertension, and dyslipidemia are frequently associated with obesity [2]. With these diseases, microvascular structures are further affected and comorbidities are observed. Besides, in the eye, age-related macular degeneration, optic neuropathy, and diabetic or hypertensive retinopathy are observed more frequently in obese individuals due to impaired microcirculation [3].

As a result of obesity treatment, microvascular diseases are less likely to occur and microcirculation is improved. Laparoscopic sleeve gastrectomy (LSG), which has recently been widely used against obesity, has been shown to reduce mortality and morbidity [4]. However, it has been reported that the severity of diabetic retinopathy paradoxically increased after bariatric surgery [5]. The presence of heterogeneous groups (different surgical procedures, different severity of diabetic retinopathy, lack of a matched non-surgical control group) may be effective in obtaining these results [6].

Studies have generally examined microcirculation and macular thickness with bariatric surgery in obese individuals with metabolic disease, but changes in microvascular structures and vessel density with surgery in individuals without metabolic disease have not been sufficiently examined [6, 7]. Obesity surgery performed in obese patients who are known to have more robust microvascular structures and who are not accompanied by diabetes, hypertension, and dyslipidemia, which are now called metabolic syndrome, can give us clearer information with more homogeneous patient groups. It may also facilitate our understanding of the impact of bariatric surgery on microvascular structures. In our study, we aimed to investigate the changes in macular vascular density by noninvasive optical coherence tomography angiography (OCTA) in obese patients without diabetes, hypertension, and dyslipidemia who underwent LSG.

This study was conducted prospectively between August 2023 and January 2024 at Harran University Faculty of Medicine, Department of Ophthalmology and General Surgery. It was conducted using OCTA measurement data of patients who underwent LSG for obesity before and 6 months after surgery. Informed written consent was obtained from all participants. The study protocol adhered to the principles of the Declaration of Helsinki.

The study included 96 eyes of 48 patients (19 men, 29 women) who had a body mass index (BMI) of ≥40 and were diagnosed as morbidly obese and underwent bariatric surgery. Complete ophthalmologic examinations including best-corrected visual acuity, and intraocular pressure measured with a Goldman applanation tonometer, slit lamp, and fundoscopic examinations were performed and recorded in the ophthalmologic clinic. Best-corrected visual acuities were evaluated using the Snellen chart.

In the bariatric unit, complete physical examinations, and anthropometric measurements including height-weight, fasting blood glucose, and blood pressure measurements were performed. Anthropometric data (weight, height) were converted to BMI for analysis according to the following formula: BMI = weight/height (kg/m2). Diabetes, hypertension, hyperlipidemia (triglycerides ≥1.70 mmol/L; low-density lipoprotein cholesterol [LDL-c] <2.6 mmol/L; high-density lipoprotein cholesterol [HDL-c] <1.04 mmol/L) constitute the metabolic syndrome. Ten patients with these metabolic diseases were excluded.

Patients with an age range of 18–60 years, best-corrected visual acuity of 20/20 or better, refractive error ±3.00, axis length between 21 and 24 mm, and intraocular pressure <21 were included in the study. Exclusion criteria were the presence of any retinopathy or neuropathy, the presence of a condition that interfered with the ambient opacity for OCT, previous refractive or intraocular surgery, history of alcohol, coffee, or cigarette addiction.

OCT Imaging Technique

OCTA imaging was performed by the same trained personnel using the Heidelberg Spectralis II OCT (Heidelberg, Germany). Images were recorded at an angle of 15 × 15° and a lateral resolution of 5.7 µm/pixel. This resulted in a retinal section of 2.9 × 2.9 mm. Data were exported and analyzed with the Erlangen-Angio-Tool (EA-Tool) software coded in MATLAB (The MathWorks, Inc.) [8]. Peripapillary and macular data on superficial vascular plexus (SVP), intermediate capillary plexus (ICP), and deep capillary plexus (DCP) were imported into the application and analyzed separately. For analysis, vessel density was calculated in 12 sectors of the macula and 4 sectors of the peripapillary region. In all, 3 circular and 12 sectoral vessel density analyses were performed for the macula and 4 for the peripapillary (shown in Fig. 1). The anatomical positioning system (part of the Glaucoma Module Premium Edition [GMPE], Heidelberg Engineering, Heidelberg, Germany) was implemented in EA-Tool. This feature aligns all OCTA scans with respect to their respective fovea-to-Bruch’s membrane opening center axis to enable better comparison of different scans. This fovea-to-Bruch’s membrane opening center axis is defined by the center of the fovea and Bruch’s membrane opening [9].

Fig. 1.

Image of macula divided into 12 sectors and peripapillary region divided into 4 sectors in obese patients. OCTA images of the superficial vascular plexus (SVP, a), intermediate capillary plexus (ICP, b), deep capillary plexus (DCP, c), and peripapillary region (d).

Fig. 1.

Image of macula divided into 12 sectors and peripapillary region divided into 4 sectors in obese patients. OCTA images of the superficial vascular plexus (SVP, a), intermediate capillary plexus (ICP, b), deep capillary plexus (DCP, c), and peripapillary region (d).

Close modal

For the retinal layers, three concentric regions were defined relative to the macular grid, centered on the umbo used by the Early Treatment Diabetic Retinopathy Study (ETDRS): fovea 1 mm in diameter, parafoveal ring 1–3 mm from the umbilicus, and perifoveal ring 3–6 mm from the umbilicus. Automated measurement of retinal thickness included in the instrument was used.

The bariatric surgery performed was sleeve gastrectomy. The stomach was removed vertically starting at a distance of 3 cm from the pylorus and 2 cm from the esophagogastric junction. Trestabler was used as a stabler. The stabler line was reinforced with omentopexy.

Statistics

In the study, the SPSS 2027 program was used for statistical analysis while evaluating the findings obtained. In the evaluation of the study data, quantitative variables were expressed as mean and standard deviation and qualitative variables were expressed as frequency and percentage using descriptive statistical methods. Shapiro-Wilks test and box plot graphs were used to analyze the conformity of the data to normal distribution. Wilcoxon signed-rank test was used for within-group evaluations of variables that did not show normal distribution. Paired-sample t test was used for within-group evaluations of variables that showed normal distribution. Spearman’s correlation analysis was used to evaluate the relationships between variables. Results were evaluated at a 95% confidence interval and significance was evaluated at p < 0.05 level.

Our study was conducted with 96 eyes of a total of 48 patients, 60.4% (n = 29) of whom were female and 39.6% (n = 19) of whom were male. The mean age of the patients who participated in the study was 39.63 ± 7.45 years. Table 1 shows the clinical and demographic characteristics of the patients before bariatric surgery. Six months postoperatively, mean BMI decreased significantly to 35.46 ± 4.26 kg/m2 compared to 48.52 ± 5.91 kg/m2 preoperatively (p < 0.05).

Table 1.

Demographic and clinical characteristics before bariatric surgery

n (%)
Sex 
 Female 29 (60.4) 
 Male 19 (39.6) 
Age, years 39.63±7.45 
Height, cm 165.73±8.39 
Weight, kg 133.71±14.31 
BMI, kg/m2 48.52±5.91 
Refractive error 
 Right eye 0.05±0.69 
 Left eye 0.25±0.58 
BCVA 
 Right eye 20/20±20/80 
 Left eye 20/20±20/160 
IOP, mm Hg 
 Right eye 18.88±2.57 
 Left eye 18.69±2.57 
Systolic BP, mm Hg 128.04±6.60 
Diastolic BP, mm Hg 80.48±6.33 
Glucose, mg/dL 95.13±11.52 
HbA1c, %, mmol/mol 5.17±0.28 
LDL cholesterol, mg/dL 151.31±17.42 
Total cholesterol, mg/dL 120.15±25.32 
HDL cholesterol, mg/dL 47.75±6.32 
Triglyceride, mg/dL 114.71±16.97 
n (%)
Sex 
 Female 29 (60.4) 
 Male 19 (39.6) 
Age, years 39.63±7.45 
Height, cm 165.73±8.39 
Weight, kg 133.71±14.31 
BMI, kg/m2 48.52±5.91 
Refractive error 
 Right eye 0.05±0.69 
 Left eye 0.25±0.58 
BCVA 
 Right eye 20/20±20/80 
 Left eye 20/20±20/160 
IOP, mm Hg 
 Right eye 18.88±2.57 
 Left eye 18.69±2.57 
Systolic BP, mm Hg 128.04±6.60 
Diastolic BP, mm Hg 80.48±6.33 
Glucose, mg/dL 95.13±11.52 
HbA1c, %, mmol/mol 5.17±0.28 
LDL cholesterol, mg/dL 151.31±17.42 
Total cholesterol, mg/dL 120.15±25.32 
HDL cholesterol, mg/dL 47.75±6.32 
Triglyceride, mg/dL 114.71±16.97 

Data are mean ± SD.

BMI, body mass index; BCVA, best-corrected visual acuity; IOP, intraocular pressure; BP, blood pressure; HbA1c, glycosylated hemoglobin; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

The mean macular vessel densities before bariatric surgery were 31.12 ± 4.32 (SVP), 22.02 ± 4.21 (ICP), and 24.12 ± 4.66 (DCP), respectively. After surgery, the mean vessel densities were 31.19 ± 4.33 (SVP), 22.08 ± 4.01 (ICP), and 26.19 ± 4.45 (DCP). There was a significant increase in vessel density in DCP 6 months after bariatric surgery (p < 0.01). Meanwhile, vessel density in SVP and ICP showed no significant difference (p>0.05). The data of the sectoral analysis and average of the vascular density (s1–s12) of SVP, ICP, and DCP before and after bariatric surgery are shown in Table 2. Comparison of mean measurements of SVP, ICP, and DCP before and after bariatric surgery is shown in Figure 2.

Table 2.

Comparison of macular SVP, ICP, and DCP in all sectors and mean before and after bariatric surgery

SVPp valueICPp valueDCPp value
before bariatric surgeryafter bariatric surgerybefore bariatric surgeryafter bariatric surgerybefore bariatric surgeryafter bariatric surgery
s1 31.22±4.49 31.28±4.44 0.379 22.23±4.05 22.32±3.97 0.140 23.97±4.89 25.71±4.61 0.001* 
s2 31.16±4.49 31.17±4.48 0.854 22.49±4.26 22.51±4.32 0.726 24.13±4.87 26.30±4.76 0.001* 
s3 31.15±4.40 31.18±4.34 0.580 23.00±4.59 23.03±4.56 0.551 26.06±4.73 28.01±4.70 0.001* 
s4 31.20±3.99 31.23±4.07 0.593 23.11±4.63 23.19±4.63 0.339 26.04±4.83 28.67±4.51 0.001* 
s5 31.23±4.47 31.26±4.53 0.593 22.50±4.58 22.46±4.50 0.468 24.18±4.83 26.61±4.47 0.001* 
s6 31.17±4.49 31.19±4.52 0.741 21.92±4.41 21.97±4.42 0.401 23.46±4.77 25.64±4.64 0.001* 
s7 31.48±4.31 31.53±4.22 0.590 21.19±4.36 21.23±4.32 0.767 23.73±4.78 25.96±4.52 0.001* 
s8 31.07±4.43 31.16±4.75 0.545 20.99±4.34 21.15±4.35 0.163 22.88±4.82 24.13±4.58 0.001* 
s9 30.69±4.26 30.84±4.60 0.132 21.24±4.16 21.18±4.15 0.617 22.84±4.86 25.11±4.59 0.001* 
s10 30.41±4.28 30.58±4.36 0.176 21.61±4.34 21.66±3.92 0.845 23.15±4.72 25.05±4.70 0.001* 
s11 31.17±4.46 31.30±4.60 0.276 21.85±4.71 22.09±3.83 0.324 24.01±4.81 26.08±4.79 0.001* 
s12 31.50±4.47 31.53±4.51 0.911 22.13±4.92 22.15±3.64 0.943 25.02±4.69 27.03±4.80 0.001* 
Mean 31.12±4.32 31.19±4.33 0.057 22.02±4.21 22.08±4.01 0.427 24.12±4.66 26.19±4.45 0.001* 
SVPp valueICPp valueDCPp value
before bariatric surgeryafter bariatric surgerybefore bariatric surgeryafter bariatric surgerybefore bariatric surgeryafter bariatric surgery
s1 31.22±4.49 31.28±4.44 0.379 22.23±4.05 22.32±3.97 0.140 23.97±4.89 25.71±4.61 0.001* 
s2 31.16±4.49 31.17±4.48 0.854 22.49±4.26 22.51±4.32 0.726 24.13±4.87 26.30±4.76 0.001* 
s3 31.15±4.40 31.18±4.34 0.580 23.00±4.59 23.03±4.56 0.551 26.06±4.73 28.01±4.70 0.001* 
s4 31.20±3.99 31.23±4.07 0.593 23.11±4.63 23.19±4.63 0.339 26.04±4.83 28.67±4.51 0.001* 
s5 31.23±4.47 31.26±4.53 0.593 22.50±4.58 22.46±4.50 0.468 24.18±4.83 26.61±4.47 0.001* 
s6 31.17±4.49 31.19±4.52 0.741 21.92±4.41 21.97±4.42 0.401 23.46±4.77 25.64±4.64 0.001* 
s7 31.48±4.31 31.53±4.22 0.590 21.19±4.36 21.23±4.32 0.767 23.73±4.78 25.96±4.52 0.001* 
s8 31.07±4.43 31.16±4.75 0.545 20.99±4.34 21.15±4.35 0.163 22.88±4.82 24.13±4.58 0.001* 
s9 30.69±4.26 30.84±4.60 0.132 21.24±4.16 21.18±4.15 0.617 22.84±4.86 25.11±4.59 0.001* 
s10 30.41±4.28 30.58±4.36 0.176 21.61±4.34 21.66±3.92 0.845 23.15±4.72 25.05±4.70 0.001* 
s11 31.17±4.46 31.30±4.60 0.276 21.85±4.71 22.09±3.83 0.324 24.01±4.81 26.08±4.79 0.001* 
s12 31.50±4.47 31.53±4.51 0.911 22.13±4.92 22.15±3.64 0.943 25.02±4.69 27.03±4.80 0.001* 
Mean 31.12±4.32 31.19±4.33 0.057 22.02±4.21 22.08±4.01 0.427 24.12±4.66 26.19±4.45 0.001* 

Paired-samples t test. Data are mean ± SD.

*p < 0.01.

Fig. 2.

Mean measurements of superficial vascular plexus (SVP), intermediate capillary plexus (ICP), and deep capillary plexus (DCP) before and after bariatric surgery.

Fig. 2.

Mean measurements of superficial vascular plexus (SVP), intermediate capillary plexus (ICP), and deep capillary plexus (DCP) before and after bariatric surgery.

Close modal

The comparison of vessel density measurements of all sectors in the peripapillary region before and after bariatric surgery is shown in Table 3. The change in mean vessel density in the peripapillary region after bariatric surgery compared to before bariatric surgery was not statistically significant (p = 0.088; p > 0.05).

Table 3.

Comparison of peripapillary vessel density measurements before and after bariatric surgery in all sectors and average

Before bariatric surgeryAfter bariatric surgeryp value
s1 30.39±3.26 30.53±3.28 b0.510 
s2 30.45±5.03 30.53±5.07 b0.088 
s3 31.50±5.24 31.52±5.14 b0.974 
s4 31.04±4.74 31.23±4.59 b0.229 
Mean 30.84±4.29 30.95±4.20 a0.088 
Before bariatric surgeryAfter bariatric surgeryp value
s1 30.39±3.26 30.53±3.28 b0.510 
s2 30.45±5.03 30.53±5.07 b0.088 
s3 31.50±5.24 31.52±5.14 b0.974 
s4 31.04±4.74 31.23±4.59 b0.229 
Mean 30.84±4.29 30.95±4.20 a0.088 

Data are mean ± SD.

aPaired-samples t test.

bWilcoxon signed-rank test.

The comparison of macular thickness measurements before and after bariatric surgery is shown in Table 4. When we compared the macular thicknesses before and after bariatric surgery, a significant increase was found in the fovea, parafovea, and perifovea (for all; p < 0.01).

Table 4.

Comparison of macular thickness measurements before and after bariatric surgery

Before bariatric surgeryAfter bariatric surgeryp value
Fovea, μm 274.31±16.68 280.61±16.47 0.001* 
Parafovea, μm 331.73±14.61 338.31±15.54 0.001* 
Perifovea, μm 295.17±18.49 298.41±17.33 0.004* 
Before bariatric surgeryAfter bariatric surgeryp value
Fovea, μm 274.31±16.68 280.61±16.47 0.001* 
Parafovea, μm 331.73±14.61 338.31±15.54 0.001* 
Perifovea, μm 295.17±18.49 298.41±17.33 0.004* 

Paired-samples t test. Data are mean ± SD.

*p < 0.01.

The correlation analysis of BMI and macular and peripapillary vessel density changes is shown in Table 5. There was no significant correlation between change in BMI after obesity compared to before obesity and mean vessel density in SVP, ICP, DCP, and peripapillary region (p > 0.05).

Table 5.

Relationship between BMI and macular and peripapillary vessel density changes

∆ BMI
∆ SVP (mean) 
r −0.061 
P 0.678 
∆ ICP (mean) 
r 0.123 
P 0.405 
∆ DCP (mean) 
r −0.060 
p 0.685 
∆ peripapillary (mean) 
r −0.257 
p 0.078 
∆ BMI
∆ SVP (mean) 
r −0.061 
P 0.678 
∆ ICP (mean) 
r 0.123 
P 0.405 
∆ DCP (mean) 
r −0.060 
p 0.685 
∆ peripapillary (mean) 
r −0.257 
p 0.078 

BMI, body mass index; SVP, superficial vascular plexus; ICP, intermediate capillary plexus; DCP, deep capillary plexus; r, Pearson correlation test.

In our study, we determined the increase in the DCP and retinal layer thickness after bariatric surgery in obese individuals without metabolic disease. There was no significant correlation between BMI changes and macular vessel density changes.

It has been reported that arteriole diameters increased, venule diameters decreased, and microvascular improvement was observed after bariatric surgery [4]. Microvascular measurements in the retina have been proven to be surrogate markers of systemic microvascular diseases and predictors of future cardiometabolic disease [4, 10, 11]. Therefore, the extent to which BMI, which decreases with bariatric surgery, affects the vascular structures in the retina is of particular importance. In many studies, OCTA has been accepted as a valuable diagnostic method to evaluate macular microvascular changes following significant weight loss [10, 12]. Previous studies evaluating vascular structures made static and manual measurements [4, 7]. The OCTA we used in our study offers the opportunity to measure dynamically and automatically thanks to its special software. In addition, the highly reliable semi-automated vessel density assessment software (EA-Tool 1.0), which we used in our study, makes it possible to detect even the smallest changes in retinal microvessel structure [8, 9].

Metabolic diseases such as diabetes, hypertension, and dyslipidemia, which are frequently associated with obesity, constitute a heterogeneous group. Depending on the frequency and severity of metabolic disease, vascular structures are affected more, and microcirculation is disrupted [6, 10]. This may prevent a clear presentation of the results and a clear understanding of the pathophysiology of the event. The extent of microvascular improvement in individuals without metabolic disease after bariatric surgery compared to those with metabolic disease is not sufficiently known. Determination of this situation will contribute to the pathophysiology of the event and will also show that microvascular structures are affected when metabolic diseases are excluded. This, in turn, may show us that BMI directly affects microvascular structures. For this reason, we did not include individuals with metabolic diseases in our study to be homogeneous in our study. There are limited number of studies investigating bariatric surgery in obese patients separated according to their metabolic status.

Carlsson et al. [13] compared microvascular disease outcomes after bariatric surgery in patients divided into groups according to baseline glycemic status (normal, prediabetes, screen-detected diabetes, and established diabetes). In their study, they showed that bariatric surgery was associated with a lower risk of microvascular disease in all patient subgroups, but the least affected group was patients with prediabetes. Chen et al. [10] classified patients according to their metabolic status (normal, metabolically healthy obese, obese with metabolic syndrome). They reported that vascular density was lowest in the group with metabolic syndrome and microvascular structures were affected due to increased BMI even in the absence of metabolic disease. In the same study, they reported that vascular density increased in all groups 6 months after bariatric surgery. Similar to our study, ElShazly et al. [14] found an increase in macular vessel density only in the DCP after bariatric surgery in patients without diabetes and hypertension. Similar to Chen et al. [10]’ s study, we concluded that the proinflammatory state associated with obesity may cause early pathological microcirculatory damage in obesity before metabolic factors. As a matter of fact, Doğan et al. [15], in their comparative study with non-obese healthy individuals, reported that the decrease in retinal vascular density and retinal thickness in obese patients was caused by obesity-related oxidative stress, increased inflammatory cytokines, and microvascular damage. There was no evidence of retinopathy in any of our patients. No signs of retinopathy developed after surgery. This suggests that bariatric surgery does not trigger the development of diabetic or hypertensive retinopathy, a finding supported by many studies [16, 17]. However, some studies have found that bariatric surgery is associated with paradoxical acute worsening of microvascular impairment [5].

We also aim to investigate the beneficial effect of bariatric surgery on the microcirculation. Therefore, when we examined retinal thickness, we found increased thickness in all retinal layers. This finding suggests that the increase in thickness of the retinal layers is due to an increase in retinal perfusion and improvement in retinal perfusion triggered by bariatric surgery, especially by an increase in the thickness of the deep vessel density, which is an abundantly vascularized tissue. As a matter of fact, some studies have found increases in different layers of the retina with obesity surgery. Laiginhas et al. [6] reported that an increase was detected in all layers of fovea, parafovea, and perifovea, and ElShazly et al. [14] reported that an increase was detected in fovea and parafovea. Laiginhas et al. [6] in a study excluding patients with diabetes, hypertension, and dyslipidemia reported that the increase in all retinal layers was independent of diabetes status and that the increase was due to increased perfusion even in the absence of metabolic disease. Likewise, in our study, we found an increase in fovea, parafovea, and perifovea independent of metabolic diseases. Gönül et al. [3] in their study investigating the efficacy of bariatric surgery in patients without diabetes and hypertension showed that microcirculation improved with surgery and there was a moderate correlation between BMI and preoperative choroidal thickness values in parallel with our study. However, unlike our study, microcirculation was evaluated with choroidal thickness measurement. The increased vascular density in the deep plexus in our results can be explained by the study of Çelik et al. [18] showing the increase in retrobulbar blood flow in obesity surgery. It has also been found that the DCP is more sensitive to pathologic conditions than the superficial plexus [19].

Another parameter we examined in our study was the peripapillary vessel density and there are limited number of studies on this subject in patients who underwent bariatric surgery. ElShazly et al. [20] reported that no change was found in optic nerve head blood flow after surgery, similar to our study. In terms of correlation, Chen et al. [10] revealed a negative correlation between superficial, deep, and mean macular vessel density and change in BMI. ElShazly et al. [14], in parallel with our study, found that there was no correlation between BMI change and superficial macular vessel density, whereas there was a correlation in deep vessel density.

Our study has several limitations. First, although patients with diabetes and hypertension were excluded, the metabolic status of obese patients before surgery was heterogeneous (duration of exposure to the high-fat diet, severity and duration of comorbidities). Second, longer follow-ups will clarify whether microvascular changes are associated with clinically significant findings. Finally, we did not exclude the possible confounding effects of diet, exercise, or other lifestyle treatments in addition to medications. Longer-term studies with larger numbers of patients are needed to eliminate the influence of these additional factors.

We observed an increase in macular vascular density in the DCP and in all retinal layers after bariatric surgery in obese patients without metabolic disease. No significant correlation was found between post-surgical BMI change and SVP, ICP, DCP, and peripapillary vessel density. Our study may provide new insights into the changes in microvascular structures after bariatric surgery and thus the underlying pathophysiological processes. It may suggest that microvascular structures are also affected in obese individuals without metabolic disease and that microperfusion improves with bariatric surgery.

We thank Mardin CY, Department of Opthalmology, Erlangen-Nürnberg University Hospital, Germany, for sharing the Erlangen-Angio-Tool program.

This study protocol was reviewed and approved by Harran University Faculty of Medicine Ethics Committee, approval number [10.07.23‐249724]. Informed written consent was obtained from all participants.

The authors have no conflicts of interest to declare.

This manuscript received no funding.

Muslum Toptan reviewed the literature and performed extensive revisions of the manuscript. Hasan Elkan reviewed the literature and wrote the first draft under the guidance of the corresponding author (M.T.).

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author.

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