Background:
It is now recognized that different metabolic tissues have important signaling contributions to the physiologic regulation of whole-body energy metabolism. For instance, the adipose tissue is no longer considered just an energy storage site but also serves as an essential source of adipokines including leptin, adiponectin, and resistin that directly influence other organs such as the brain and liver to elicit significant effects on global glucose and lipid metabolism. Similarly, the heart is emerging not simply as a pumping engine but an important endocrine organ that can secrete soluble factors acting on peripheral tissues such as the adipose tissue to maintain normal systemic energy homeostasis. For instance, cardiac-released natriuretic peptides increase glucogenesis in the liver and regulate lipolysis and promote thermogenesis in the adipose tissue. In addition to the understanding that individual tissue can serve as an important integrator of systemic metabolic physiology, each tissue system can also play an important role in the endocrine regulation of systemic energy homeostasis under conditions of physiologic (fasting, exercise) or pathological (diet-induced obesity, diabetes) stress. For instance, the heart may regulate adipose tissue and liver function via the cardiac-specific action of the mediator complex subunit 13 that in turn promotes resistance against high fat diet-induced obesity and improve insulin sensitivity. In addition, the adipose transcription factor Kruppel-like factor 15 (KLF15) plays an important role in the regulation of skeletal muscle performance and liver ketogenesis under condition of fasting.
Author Guidelines:
This Research Topic will focus on how different organ systems (such as adipose tissue, heart, liver, or skeletal muscle) can mediate important endocrine regulation of systemic energy homeostasis under normal condition and conditions of physiologic or pathological metabolic stresses. For example, one concept that can be discussed under this Topic is that a tissue system (for eg., heart or adipose tissue) can adaptively respond to physiologic or pathologic stresses by evoking compensatory gene expression and signaling pathway changes within itself as well as in other tissues, thereby contributing to a heightened ability of the body to counteract stress and allowing maintenance of normal systemic energy homeostasis under stressed condition.
Specific Guidelines:
For regulation of physiologic energy metabolism, identify the tissue of interest and describe how perturbation of gene or signaling pathway activity in that tissue (for eg., by tissue-specific genetic overexpression or inhibition) could impact another or other tissue(s) (metabolic gene expression changes, lipid accumulation, cytoskeletal disorganization etc.) to affect energy metabolic physiology in a systemic manner (circulating metabolite level changes, exercise endurance etc.).
For pathologic regulation of energy metabolism, identify a tissue of interest and a metabolic stress (diet-induced obesity or fasting) and describe the response of that tissue to the stress (for eg., induction of a gene or signaling pathway in response to stress). Describe how the molecular changes in that tissue induced by stress exposure can cause molecular and structural changes in another tissue that would attenuate the stress (adaptive responses) or exacerbate the stress (maladaptive responses) in a tissue-intrinsic and systemic level.
Background:
It is now recognized that different metabolic tissues have important signaling contributions to the physiologic regulation of whole-body energy metabolism. For instance, the adipose tissue is no longer considered just an energy storage site but also serves as an essential source of adipokines including leptin, adiponectin, and resistin that directly influence other organs such as the brain and liver to elicit significant effects on global glucose and lipid metabolism. Similarly, the heart is emerging not simply as a pumping engine but an important endocrine organ that can secrete soluble factors acting on peripheral tissues such as the adipose tissue to maintain normal systemic energy homeostasis. For instance, cardiac-released natriuretic peptides increase glucogenesis in the liver and regulate lipolysis and promote thermogenesis in the adipose tissue. In addition to the understanding that individual tissue can serve as an important integrator of systemic metabolic physiology, each tissue system can also play an important role in the endocrine regulation of systemic energy homeostasis under conditions of physiologic (fasting, exercise) or pathological (diet-induced obesity, diabetes) stress. For instance, the heart may regulate adipose tissue and liver function via the cardiac-specific action of the mediator complex subunit 13 that in turn promotes resistance against high fat diet-induced obesity and improve insulin sensitivity. In addition, the adipose transcription factor Kruppel-like factor 15 (KLF15) plays an important role in the regulation of skeletal muscle performance and liver ketogenesis under condition of fasting.
Author Guidelines:
This Research Topic will focus on how different organ systems (such as adipose tissue, heart, liver, or skeletal muscle) can mediate important endocrine regulation of systemic energy homeostasis under normal condition and conditions of physiologic or pathological metabolic stresses. For example, one concept that can be discussed under this Topic is that a tissue system (for eg., heart or adipose tissue) can adaptively respond to physiologic or pathologic stresses by evoking compensatory gene expression and signaling pathway changes within itself as well as in other tissues, thereby contributing to a heightened ability of the body to counteract stress and allowing maintenance of normal systemic energy homeostasis under stressed condition.
Specific Guidelines:
For regulation of physiologic energy metabolism, identify the tissue of interest and describe how perturbation of gene or signaling pathway activity in that tissue (for eg., by tissue-specific genetic overexpression or inhibition) could impact another or other tissue(s) (metabolic gene expression changes, lipid accumulation, cytoskeletal disorganization etc.) to affect energy metabolic physiology in a systemic manner (circulating metabolite level changes, exercise endurance etc.).
For pathologic regulation of energy metabolism, identify a tissue of interest and a metabolic stress (diet-induced obesity or fasting) and describe the response of that tissue to the stress (for eg., induction of a gene or signaling pathway in response to stress). Describe how the molecular changes in that tissue induced by stress exposure can cause molecular and structural changes in another tissue that would attenuate the stress (adaptive responses) or exacerbate the stress (maladaptive responses) in a tissue-intrinsic and systemic level.