Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.06.08.730805

Higher baseline levels of fatty acid esters of hydroxy fatty acids do not further enhance the stimulatory effect of regular exercise on insulin sensitivity in obese mice

Abstract

BackgroundExercise is an effective way to improve metabolic health, and the modulation of adipose tissue (AT) secretory functions may play a significant role in this process. AT produces various lipokines, including fatty acid esters of hydroxy fatty acids (FAHFA), which increase insulin sensitivity and have anti-inflammatory effects. While factors such as sex, age, obesity, and genetics influence FAHFA levels, their impact on exercise-induced FAHFA regulation remains unclear. MethodsFirst, sex-specific responses to an acute bout of exercise were assessed in wild-type (WT) and ADTRP-deficient (ADTRP KO) mice. Fasted mice underwent acute treadmill exercise until exhaustion, followed by analysis of non-esterified fatty acids in plasma, ex vivo lipolysis in the presence or absence of a hormone-sensitive lipase (HSL) inhibitor, and FAHFA release from AT (measured by LC-MS). Second, obese male WT and ADTRP KO mice fed a high-fat diet underwent 7 weeks of regular treadmill exercise (5 days/week), after which parameters of glucose homeostasis, plasma and AT FAHFA levels, and AT lipid profiles were analyzed. ResultsAcute exercise-induced increases in plasma non-esterified fatty acid levels, AT lipolysis, and FAHFA release from AT explants were more pronounced in male mice of both genotypes. Conversely, pharmacological inhibition of HSL using BAY 59-9435 increased FAHFA release from AT explants only in females. In obese sedentary ADTRP KO mice, insulin sensitivity was improved compared with their WT counterparts. Although regular exercise suppressed weight gain in obese animals of both genotypes, insulin sensitivity improved only in WT mice. Chronic exercise generally had no effect on plasma FAHFA levels in mice fed ad libitum; however, in WT mice, it increased the levels of FAHFA-containing triacylglycerol estolides, which were associated with improved insulin sensitivity. ConclusionsAcute exercise revealed sex-specific differences in AT lipolysis and FAHFA metabolism, with HSL playing an important role in FAHFA hydrolysis. Chronic exercise in obesity increases insulin sensitivity and FAHFA storage in AT; however, this effect is absent in ADTRP KO mice, which exhibit elevated FAHFA levels in AT, a condition associated with improved insulin sensitivity even in non-exercising animals.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Mitrovic, M., Horakova, O., Riecan, M., Kleinova, V., Zouhar, P., Cajka, T., Kuda, O., Rossmeislova, L., Rossmeisl, M.. 2026-06-11. Higher baseline levels of fatty acid esters of hydroxy fatty acids do not further enhance the stimulatory effect of regular exercise on insulin sensitivity in obese mice. https://doi.org/10.64898/2026.06.08.730805

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Thoracoabdominal pressure transmission during prone and supine cardiopulmonary resuscitation in fresh-frozen human cadavers

Background: Prone cardiopulmonary resuscitation (CPR) may be necessary when turning a prone patient supine would delay chest compressions. Although prone compressions can generate arterial pressures comparable with or greater than supine CPR, the pathway of pressure transmission is uncertain. We examined synchronized intrathoracic, intra-abdominal, and central arterial pressures in both supine and prone positions. Methods: Two thawed fresh-frozen adult cadavers underwent three, 2-minute mechanical CPR trials per position in a counterbalanced crossover sequence. Solid-state catheters recorded pleural, peritoneal, and central arterial pressures simultaneously. Trial-level outcomes included peak pressure, mean pressure, pressure-time area, and the mean peritoneal-to-pleural pressure gradient. Exploratory fixed-effects models included position, cadaver, and their interaction. Results: Prone CPR increased peak intrathoracic pressure by 7.04 mmHg, peak intra-abdominal pressure by 21.69 mmHg, and peak arterial pressure by 15.40 mmHg. Mean intra-abdominal and arterial pressures increased by 16.22 and 9.90 mmHg, respectively. The mean peritoneal-to-pleural gradient reversed direction from -8.46 mmHg supine to 4.85 mmHg prone. Intrathoracic pressure-time area increased 3.4-fold, from 1.62 to 5.46 mmHg{middle dot}s, and arterial pressure-time area increased 2.2-fold, from 2.96 to 6.42 mmHg{middle dot}s. Conclusions: Compared to supine, prone mechanical CPR generated higher arterial pressures and reversed the pressure relationship across the thoracoabdominal boundary in both cadavers. Higher abdominal pressure coincided with a larger intrathoracic pressure-time area, a pattern compatible with reduced caudal pressure dissipation.

physiology↗

Hypothalamic Farnesoid X Receptor deficiency alters energy balance by modulating hepatic glucose production and adipose tissue metabolism through central insulin signaling.

Objectives: The bile acid nuclear receptor Farnesoid X Receptor (FXR, NR1H4) is a major regulator of metabolism and energy homeostasis in peripheral organs. It modulates bile acid, glucose, and lipid metabolism, as well as fat mass and body weight. However, FXR is also expressed in the brain, particularly in the hypothalamus, a key center for the regulation of energy homeostasis. Although one study has demonstrated a role for brain FXR activation in energy balance, its specific hypothalamic role is still unknown. Here, we examined the role of FXR in the mediobasal hypothalamus in the regulation of energy balance. Methods: We used a genetic approach combined with metabolic phenotyping to determine the effect of FXR invalidation in the mediobasal hypothalamus on metabolic parameters involved in the central regulation of energy homeostasis. Results: Our results demonstrate that hypothalamic FXR deficiency induces a positive energy balance, resulting in a reduction in energy expenditure due to alterations in glucose metabolism accompanied by structural changes in white adipose tissues. Conclusion: This study uncovers a previously unrecognized role for hypothalamic FXR in the central homeostatic control of energy balance, providing new insights into its contribution to peripheral glucose metabolism and adipose tissue structural remodeling.

physiology↗

Rad and Phospholamban are Key Drivers of the Ventricular Adrenergic Response and Stress-Induced Arrhythmia

The adrenergic response is a fundamental mechanism that regulates heart rate (chronotropy), cardiac contractility (inotropy) and relaxation (lusitropy). Adrenergic stress is also a recognized trigger of arrhythmia in disease. Yet, our understanding of the underlying molecular basis remains incomplete. Protein kinase A (PKA) and the calcium/calmodulin-dependent kinase II (CaMKII) phosphorylate multiple targets proposed to participate in the adrenergic response, including the GTP-binding protein Rad, phospholamban (PLB) and ryanodine receptor 2 (RyR2). Here we demonstrate that phosphorylation of both Rad and PLB is necessary for inotropy and lusitropy. We show that changes in cardiac contractility and relaxation are primarily dependent on intracellular calcium handling. Finally, we report that Rad and PLB control stress-induced arrhythmogenesis, despite the phosphorylation of other pro-arrhythmic targets. We have identified the essential molecular components of the adrenergic response, resolving a long-standing debate in cardiac excitation-contraction coupling and refining current models of sympathetic regulation in health and disease.

physiology↗