Young Women Are Protected Against Vascular Insulin Resistance Induced by Adoption of an Obesogenic Lifestyle

Smith, James; Soares, Rogério N.; McMillan, N. J.; Jurrissen, Thomas J.; Martinez‐Lemus, Luis A.; Padilla, Jaume; Manrique‐Acevedo, Camila

doi:10.1210/endocr/bqac137

Cited by 6 publications

(4 citation statements)

References 50 publications

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“…Meda et al (137) did report an increase in Enho mRNA expression in estrogen-treated ovariectomized mice. Despite the role of estrogen signaling in the regulation of hepatic Enho mRNA expression, males have higher circulating concentrations of adropin (21,29,138), however, this has not been universally reported (28,(139)(140)(141). Moreover, Choi et al (142) have reported that T2D females exhibit higher adropin concentrations than their male T2D counterparts.…”

Section: Hepatic Enho Regulationmentioning

confidence: 99%

“…In addition to the impact of dietary fat on adropin, there is an inverse relationship between carbohydrate consumption and adropin concentrations (138). Moreover, Smith et al (141) reported increased carbohydrate consumption coupled with decreased physical activity induced a reduction in circulating adropin in males, but not females. Upon further interrogation of the influence of carbohydrate consumption on circulating adropin demonstrated that glucose induced a reduction of circulating adropin, while fructose increased circulating adropin (143).…”

Section: Circulating Adropinmentioning

confidence: 99%

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Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Jurrissen

Ramirez‐Perez

Cabral-Amador

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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Adropin is a peptide largely secreted by the liver and known to regulate energy homeostasis; however, it also exerts cardiovascular effects. Herein, we tested the hypothesis that low circulating levels of adropin in obesity and type 2 diabetes (T2D) contribute to arterial stiffening. In support of this hypothesis, we report that obesity and T2D is associated with reduced levels of adropin (in liver and plasma) and increased arterial stiffness in mice and humans. Establishing causation, we show that mesenteric arteries from adropin knockout mice are also stiffer, relative to arteries from wild-type counterparts, thus recapitulating the stiffening phenotype observed in T2D db/db mice. Given the above, we performed a set of follow-up experiments, in which we found that: 1) exposure of endothelial cells or isolated mesenteric arteries from db/db mice to adropin reduces filamentous actin (F-actin) stress fibers and stiffness; 2) adropin-induced reduction of F-actin and stiffness in endothelial cells and db/db mesenteric arteries is abrogated by inhibition of nitric oxide (NO) synthase; and 3) stimulation of smooth muscle cells or db/db mesenteric arteries with a NO mimetic reduces stiffness. Last, we demonstrated that in vivo treatment of db/db mice with adropin for four weeks reduces stiffness in mesenteric arteries. Collectively, these findings indicate that adropin can regulate arterial stiffness, likely via endothelial-derived NO, and thus support the notion that "hypoadropinemia" should be considered as a putative target for the prevention and treatment of arterial stiffening in obesity and T2D.

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Section: Hepatic Enho Regulationmentioning

confidence: 99%

Section: Circulating Adropinmentioning

confidence: 99%

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Jurrissen

Ramirez‐Perez

Cabral-Amador

et al. 2022

American Journal of Physiology-Heart and Circulatory Physiology

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“…Premenopausal women have previously been shown to be protected against other insulin resistance-inducing behaviours, namely consuming sugar sweetened beverages and reducing the daily physical activity over 10 days, compared to men. 158 Thus, future studies should specifically explore whether there are sex differences in the metabolic responses to sleep restriction and sleep restriction with exercise. It is also plausible that an un-measured attribute strongly related to obesity such as low cardiorespiratory fitness may explain the inability of exercise to rescue the cardiometabolic impairments caused by sleep restriction in individuals with obesity.…”

Section: The Role Of Physical Exercise In the Association Of Poor Sle...mentioning

confidence: 99%

“…Of note, this was the first sleep restriction and exercise study completed in individuals with obesity, it appears to be the only one to date to also include women. Premenopausal women have previously been shown to be protected against other insulin resistance‐inducing behaviours, namely consuming sugar sweetened beverages and reducing the daily physical activity over 10 days, compared to men 158 . Thus, future studies should specifically explore whether there are sex differences in the metabolic responses to sleep restriction and sleep restriction with exercise.…”

Section: The Role Of Physical Exercise In the Association Of Poor Sle...mentioning

confidence: 99%

The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review

Rogers

Banks

Jenkins

2023

Diabetes Metabolism Res

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Sleep deficiency is a ubiquitous phenomenon among Americans. In fact, in the United States, ∼78% of teens and 35% of adults currently get less sleep than recommended for their age‐group, and the quality of sleep appears to be getting worse for many. The consequences of sleep disruption manifest in a myriad of ways, including insulin resistance and disrupted nutrient metabolism, dysregulation of hunger and satiety, and potentially increased body weight and adiposity. Consequently, inadequate sleep is related to an increased risk of various cardiometabolic diseases, including obesity, diabetes, and heart disease. Exercise has the potential to be an effective therapeutic to counteract the deleterious effects of sleep disruption listed above, whereas chronic psychosocial stress may causally promote sleep disruption and cardiometabolic risk. Here, we provide a narrative review of the current evidence on the consequences of short sleep duration and poor sleep quality on substrate metabolism, circulating appetite hormones, hunger and satiety, and weight gain. Secondly, we provide a brief overview of chronic psychosocial stress and its impact on sleep and metabolic health. Finally, we summarise the current evidence regarding the ability of exercise to counteract the adverse metabolic health effects of sleep disruption. Throughout the review, we highlight areas where additional interrogation and future exploration are necessary.

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Resistance exercise breaks during prolonged sitting augment the blood flow response to a subsequent oral glucose load in sedentary adults

Rogers,

Banks,

Trachta

et al. 2024

Experimental Physiology

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Sitting‐induced impairments in postprandial blood flow are an important link between sedentary behaviour and cardiometabolic disease risk. The objective of this work was to examine the effects of resistance exercise breaks (REB) performed every 30 min during an otherwise sedentary 3‐h period on the vasodilatory response to a subsequent oral glucose load in sedentary adults. Twenty‐four sedentary adults (27 ± 7 years, 16 females) completed two conditions. Fasting blood glucose, insulin, popliteal artery blood flow (PABF) and gastrocnemius perfusion were measured immediately before standardized breakfast consumption. After breakfast, the 3‐h REB or uninterrupted (SIT) intervention period commenced. Participants sat at a workstation, and popliteal artery shear rate (PASR) was measured 60 and 120 min into this period. In the REB condition, participants performed a 3‐min REB (3 × [20 s squats, 20 s high knees, 20 s calf raises]) every 30 min. Following the intervention period, baseline measurements were repeated. Participants then consumed a 75 g glucose beverage, and PABF and perfusion were measured every 30–60 min for the following 120 min. Relative to SIT, REB increased PASR at 60 min (+31.4 ± 9.2/s, P = 0.037) and 120 min (+37.4 ± 10.2/s, P = 0.019) into the intervention period. Insulin and glucose increased (P < 0.001) in response to glucose consumption, with no differences between conditions (P ≥ 0.299). In response to the glucose load, perfusion (1.57 vs. 1.11 mL/100 mL/min, P = 0.023) and PABF (+45.3 ± 11.8 mL/min, P = 0.001) were greater after REB versus SIT. Performing 3‐min REB every 30 min during an otherwise sedentary 3‐h period augmented leg blood flow responses to an oral glucose load.Highlights What is the central question of this study?Can 3‐min resistance exercise breaks (REB) performed during an otherwise sedentary 3‐h period augment the vasodilatory response to a subsequent oral glucose load in sedentary adults? What is the main finding and its importance?Performing 3‐min REB, which included squats, high knees, and calf raises, every 30 min augmented lower limb blood flow responses to a subsequent oral glucose load compared to 3 h of uninterrupted sitting in sedentary adults. Sitting‐induced impairment in postprandial vasodilatory function has been identified as a link between sedentary behaviour and cardiometabolic disease. Thus, the current study presents a potentially effective strategy to offset this risk.

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Young Women Are Protected Against Vascular Insulin Resistance Induced by Adoption of an Obesogenic Lifestyle

Cited by 6 publications

References 50 publications

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

Role of adropin in arterial stiffening associated with obesity and type 2 diabetes

The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review

Resistance exercise breaks during prolonged sitting augment the blood flow response to a subsequent oral glucose load in sedentary adults

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