Sympathetic circuits regulating hepatic glucose metabolism: where we stand

Zsombok, Andrea; Desmoulins, Lucie; Derbenev, Andrei V.

doi:10.1152/physrev.00005.2023

Cited by 11 publications

(2 citation statements)

References 166 publications

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“…53 To this end, it regulates key processes in adipose tissue (eg, increasing thermogenesis and lipolysis), the liver (eg, promoting glycogenolysis), skeletal muscle (eg, enhancing glucose metabolism and access to substrate), and the pancreas (eg, inhibiting insulin release). [54][55][56] Metabolic functions are also influenced by the PNS through its inhibition of hepatic glucose production, pancreatic release of insulin, stimulation of nutrient absorption and utilization by the digestive organs, such as the stomach and intestines, facilitation of glycogenesis in the liver and muscles, as well as lipogenesis in adipose tissue. 43,54 It should be noted that the interplay between the SNS and PNS in metabolic homeostasis is dynamic and context dependent.…”

Section: Autonomic Regulation Of Metabolismmentioning

confidence: 99%

Neural Circuits Underlying Reciprocal Cardiometabolic Crosstalk: 2023 Arthur C. Corcoran Memorial Lecture

Rahmouni

2024

Hypertension

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The interplay of various body systems, encompassing those that govern cardiovascular and metabolic functions, has evolved alongside the development of multicellular organisms. This evolutionary process is essential for the coordination and maintenance of homeostasis and overall health by facilitating the adaptation of the organism to internal and external cues. Disruption of these complex interactions contributes to the development and progression of pathologies that involve multiple organs. Obesity-associated cardiovascular risks, such as hypertension, highlight the significant influence that metabolic processes exert on the cardiovascular system. This cardiometabolic communication is reciprocal, as indicated by substantial evidence pointing to the ability of the cardiovascular system to affect metabolic processes, with pathophysiological implications in disease conditions. In this review, I outline the bidirectional nature of the cardiometabolic interaction, with special emphasis on the impact that metabolic organs have on the cardiovascular system. I also discuss the contribution of the neural circuits and autonomic nervous system in mediating the crosstalk between cardiovascular and metabolic functions in health and disease, along with the molecular mechanisms involved.

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Section: Autonomic Regulation Of Metabolismmentioning

confidence: 99%

Neural Circuits Underlying Reciprocal Cardiometabolic Crosstalk: 2023 Arthur C. Corcoran Memorial Lecture

Rahmouni

2024

Hypertension

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“…These neurons receive synaptic projections from multiple brainstem and forebrain regions, including the respiratory neurons of the preBötC, indicating that this region integrates sympathetic control with other physiological systems (Guyenet, 2006 ). The sympathetic nervous system also regulates the energy expenditure and O 2 demand of the body by controlling peripheral (e.g., cutaneous) blood flow and heat exchange with the environment, regulating non‐shivering thermogenesis through innervations to the brown adipose tissue and stimulating lipolysis and glycogenolysis (Madden & Morrison, 2005 ; Zsombok et al., 2023 ).…”

Section: Oxygen Homeostasis and The Respiratory And Autonomic Adjustm...mentioning

confidence: 99%

Hypoxia sensing in the body: An update on the peripheral and central mechanisms

Zoccal,

Vieira,

Mendes

et al. 2023

Experimental Physiology

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An adequate supply of O2 is essential for the maintenance of cellular activity. Systemic or local hypoxia can be experienced during decreased O2 availability or associated with diseases, or a combination of both. Exposure to hypoxia triggers adjustments in multiple physiological systems in the body to generate appropriate homeostatic responses. However, with significant reductions in the arterial partial pressure of O2, hypoxia can be life‐threatening and cause maladaptive changes or cell damage and death. To mitigate the impact of limited O2 availability on cellular activity, O2 chemoreceptors rapidly detect and respond to reductions in the arterial partial pressure of O2, triggering orchestrated responses of increased ventilation and cardiac output, blood flow redistribution and metabolic adjustments. In mammals, the peripheral chemoreceptors of the carotid body are considered to be the main hypoxic sensors and the primary source of excitatory feedback driving respiratory, cardiovascular and autonomic responses. However, current evidence indicates that the CNS contains specialized brainstem and spinal cord regions that can also sense hypoxia and stimulate brain networks independently of the carotid body inputs. In this manuscript, we review the discoveries about the functioning of the O2 chemoreceptors and their contribution to the monitoring of O2 levels in the blood and brain parenchyma and mounting cardiorespiratory responses to maintain O2 homeostasis. We also discuss the implications of the chemoreflex‐related mechanisms in paediatric and adult pathologies.

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Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues

Fang,

Raza,

Song

et al. 2024

ESC Heart Failure

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Systemic aging influences various physiological processes and contributes to structural and functional decline in cardiac tissue. These alterations include an increased incidence of left ventricular hypertrophy, a decline in left ventricular diastolic function, left atrial dilation, atrial fibrillation, myocardial fibrosis and cardiac amyloidosis, elevating susceptibility to chronic heart failure (HF) in the elderly. Age‐related cardiac dysfunction stems from prolonged exposure to genomic, epigenetic, oxidative, autophagic, inflammatory and regenerative stresses, along with the accumulation of senescent cells. Concurrently, age‐related structural and functional changes in the vascular system, attributed to endothelial dysfunction, arterial stiffness, impaired angiogenesis, oxidative stress and inflammation, impose additional strain on the heart. Dysregulated mechanosignalling and impaired nitric oxide signalling play critical roles in the age‐related vascular dysfunction associated with HF. Metabolic aging drives intricate shifts in glucose and lipid metabolism, leading to insulin resistance, mitochondrial dysfunction and lipid accumulation within cardiomyocytes. These alterations contribute to cardiac hypertrophy, fibrosis and impaired contractility, ultimately propelling HF. Systemic low‐grade chronic inflammation, in conjunction with the senescence‐associated secretory phenotype, aggravates cardiac dysfunction with age by promoting immune cell infiltration into the myocardium, fostering HF. This is further exacerbated by age‐related comorbidities like coronary artery disease (CAD), atherosclerosis, hypertension, obesity, diabetes and chronic kidney disease (CKD). CAD and atherosclerosis induce myocardial ischaemia and adverse remodelling, while hypertension contributes to cardiac hypertrophy and fibrosis. Obesity‐associated insulin resistance, inflammation and dyslipidaemia create a profibrotic cardiac environment, whereas diabetes‐related metabolic disturbances further impair cardiac function. CKD‐related fluid overload, electrolyte imbalances and uraemic toxins exacerbate HF through systemic inflammation and neurohormonal renin‐angiotensin‐aldosterone system (RAAS) activation. Recognizing aging as a modifiable process has opened avenues to target systemic aging in HF through both lifestyle interventions and therapeutics. Exercise, known for its antioxidant effects, can partly reverse pathological cardiac remodelling in the elderly by countering processes linked to age‐related chronic HF, such as mitochondrial dysfunction, inflammation, senescence and declining cardiomyocyte regeneration. Dietary interventions such as plant‐based and ketogenic diets, caloric restriction and macronutrient supplementation are instrumental in maintaining energy balance, reducing adiposity and addressing micronutrient and macronutrient imbalances associated with age‐related HF. Therapeutic advancements targeting systemic aging in HF are underway. Key approaches include senomorphics and senolytics to limit senescence, antioxidants targeting mitochondrial stress, anti‐inflammatory drugs like interleukin (IL)‐1β inhibitors, metabolic rejuvenators such as nicotinamide riboside, resveratrol and sirtuin (SIRT) activators and autophagy enhancers like metformin and sodium‐glucose cotransporter 2 (SGLT2) inhibitors, all of which offer potential for preserving cardiac function and alleviating the age‐related HF burden.

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Sympathetic circuits regulating hepatic glucose metabolism: where we stand

Cited by 11 publications

References 166 publications

Neural Circuits Underlying Reciprocal Cardiometabolic Crosstalk: 2023 Arthur C. Corcoran Memorial Lecture

Neural Circuits Underlying Reciprocal Cardiometabolic Crosstalk: 2023 Arthur C. Corcoran Memorial Lecture

Hypoxia sensing in the body: An update on the peripheral and central mechanisms

Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues

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