Lytle, Kelli

Adipose tissue functions as both a storage depot and endocrine organ and is robustly responsive to a nutrient challenge by increasing blood flow. Alterations in adipose tissue blood flow (ATBF) have been described in conditions of metabolic dysfunction. We hypothesized that aging is associated with decreased perfusion to adipose tissue and that normal weight older adults would have decreased basal and glucose challenged ATBF responsiveness and conductance. We recruited 10 (6F/ 4M) generally healthy, non-diabetic, normal weights subjects aged 18-35 years (Younger YO) and 5 (3F/2M) aged 65 to 80 years (Older adults OA). Volunteers had a DEXA scan; the day of the study, volunteers arrived fasted to the clinical research unit and rested for 30 minutes, before starting ATBF measurements using the xenon washout method. ATBF and blood pressures was measured for 30 minutes at rest (baseline) and at 20, 30, and 60 minutes after ingestion of a 75 g glucose drink. We additionally measured fasting and postprandial plasma insulin concentrations (µIU/mL). Compared to the YO, older volunteers had a slightly elevated mean BMI (25.0 ±0.9 vs. 22.4 ±2.1 kg/m 2 , OA vs YO respectively p < 0.05), total body fat (26±7.4 vs. 17±4.6 kg, p < 0.05), upper body fat (8.7±2.8 vs. 5.1±2.1 kg, p < 0.05) and supine resting systolic pressure (136±18.5 107±11.4 mmHg, p < 0.05 ) compared to YO. Although not statistically significant, YO appeared to have a higher median fasting ATBF at baseline (2.8 ± 3.8 vs 1.8±4.3 ml/100g/min, YO vs. OA, respectively) and in response to the glucose challenge at T20 (3.5±2.7 vs 1.7±2.3), T30 (4.2±3.6 vs 1.8±5.2) and T60 (4.2±4.9 vs 1.4±3.9) compared to OA. Because OA appeared to have lower fasting ATBF, we examined whether ATBF responsivity (percent change from baseline) was altered in OA compared to YO. Compared to baseline, YO adults had a +13% at T20, +43% at T30 and +53% at T60. Conversely, OA had a decrease of 31% at T20, and +11% at T30, and +5% at T60. To account for the higher systolic blood pressure in OA we calculated conductance (ATBF/mean arterial pressure (MAP)) at each timepoint. Conductance was not statistically different between YO and OA at baseline, T20, T30 and T60. Interestingly, ATBF was negatively correlated to total upper body fat in both YO (r = 0.74, p< 0.05) and OA (r =0.67, p=.18). OA had higher fasting insulin concentrations than YO and in early response to OGTT at T20 but not at other timepoints. Plasma insulin was not related to either absolute or responsivity of ATBF at any timepoint. In this ongoing study, our preliminary data suggests that during fasting and in response to a 75 gm OGTT challenge, ATBF responsiveness may be altered in older adults. This suggests that reductions in adipose tissue perfusion and responsivity of perfusion in response to a stimulus known to increase adipose tissue blood flow may be impaired in older adults. Even within this normal weight population there was a strong relationship between upper body fat and ATBF. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

The role of adipose tissue (AT) inflammation in AT function in humans is unclear. We tested whether AT macrophage (ATM) content, cytokine gene expression, and senescent cell burden (markers of AT inflammation) predict AT insulin resistance measured as the insulin concentration that suppresses lipolysis by 50% (IC50). We studied 86 volunteers with normal weight or obesity at baseline and a subgroup of 25 volunteers with obesity before and after weight loss. There was a strong positive relationship between IC50 and abdominal subcutaneous and femoral fat cell size (FCS). The positive, univariate relationships between IC50 and abdominal AT inflammatory markers CD68, CD14, CD206 ATM/100 adipocytes, senescent cells, IL-6, and TNF-α mRNA were not significant after adjustment for FCS. A 10% weight loss significantly reduced IC50; however, there was no reduction in adipose ATM content, senescent cells, or cytokine gene expression. Our study suggests that commonly used markers of AT inflammation are not causally linked to AT insulin resistance, whereas FCS is a strong predictor of AT insulin resistance with respect to lipolysis.