TY - JOUR AB - Astrocytes, once viewed primarily as supportive cells in the central nervous system, are increasingly recognized as dynamic regulators in the regulation of systemic metabolism, especially within the hypothalamus. Recent research highlights their capacity to sense and integrate nutrient, hormonal, and circadian signals, modulate hypothalamic circuits, and ultimately influence whole-body energy balance. In this review, we discuss emerging studies that explore how hypothalamic astrocytes regulate glucose and lipid metabolism through neuroendocrine and autonomic pathways that extend their influence to peripheral organs. We examine emerging evidence showing that astrocytes contribute to glycemic control via glucose sensing, intracellular metabolic shifts, and modulation of key neuronal circuits. Similarly, recent investigations have identified roles for astrocytes in the regulation of adipose tissue function and body weight, particularly in the context of high-fat diet exposure, largely through their influence on hypothalamic neuron-astrocyte interactions and sympathetic output. We further consider recent findings implicating astrocytic circadian pathways in the coordination of metabolic rhythms, as well as the long-term consequences of early-life nutritional exposures, that may epigenetically program hypothalamic astrocyte function. New insights also point to region-specific and sex-dependent astrocytic functions. Together, this growing body of work positions hypothalamic astrocytes as integrators of brain-body communication in the control of energy homeostasis and highlights their potential relevance in the pathophysiology of obesity and metabolic disease. AU - Le Thuc, O. AU - Lechner, F. AU - García-Cáceres, C. C1 - 75771 C2 - 57971 CY - One New York Plaza, Suite 4600, New York, Ny, United States TI - Hypothalamic astrocytes: Connecting brain and periphery in metabolic control. JO - Rev. Endocr. Metab. Disord. PB - Springer PY - 2025 SN - 1389-9155 ER - TY - JOUR AB - The prefrontal cortex is appreciated as a key neurobiological player in human eating behavior. A special focus is herein dedicated to the dorsolateral prefrontal cortex (DLPFC), which is critically involved in executive function such as cognitive control over eating. Persons with obesity display hypoactivity in this brain area, which is linked to overconsumption and food craving. Contrary to that, higher activity in the DLPFC is associated with successful weight-loss and weight-maintenance. Transcranial direct current stimulation (tDCS) is a non-invasive neurostimulation tool used to enhance self-control and inhibitory control. The number of studies using tDCS to influence eating behavior rapidly increased in the last years. However, the effectiveness of tDCS is still unclear, as studies show mixed results and individual differences were shown to be an important factor in the effectiveness of non-invasive brain stimulation. Here, we describe the current state of research of human studies using tDCS to influence food intake, food craving, subjective feeling of hunger and body weight. Excitatory stimulation of the right DLPFC seems most promising to reduce food cravings to highly palatable food, while other studies provide evidence that stimulating the left DLPFC shows promising effects on weight loss and weight maintenance, especially in multisession approaches. Overall, the reported findings are heterogeneous pointing to large interindividual differences in tDCS responsiveness. AU - Ester-Nacke, T. AU - Kullmann, S. C1 - 63721 C2 - 51750 TI - Neurobiological regulation of eating behavior: Evidence based on non-invasive brain stimulation. JO - Rev. Endocr. Metab. Disord. PY - 2021 SN - 1389-9155 ER - TY - JOUR AB - Immune cells are present in the adipose tissue (AT) and regulate its function. Under lean conditions, immune cells predominantly of type 2 immunity, including eosinophils, M2-like anti-inflammatory macrophages and innate lymphoid cells 2, contribute to the maintenance of metabolic homeostasis within the AT. In the course of obesity, pro-inflammatory immune cells, such as M1-like macrophages, prevail in the AT. Inflammation in the obese AT is associated with the development of metabolic complications such as insulin resistance, type 2 diabetes and cardiovascular disease. Thus, the immune cell-adipocyte crosstalk in the AT is an important regulator of AT function and systemic metabolism. We discuss herein this crosstalk with a special focus on the role of innate immune cells in AT inflammation and metabolic homeostasis in obesity. AU - Chung, K.-J. AU - Nati, M.* AU - Chavakis, T. AU - Chatzigeorgiou, A.* C1 - 54993 C2 - 45967 CY - 233 Spring St, New York, Ny 10013 Usa SP - 283-292 TI - Innate immune cells in the adipose tissue. JO - Rev. Endocr. Metab. Disord. VL - 19 IS - 4 PB - Springer PY - 2018 SN - 1389-9155 ER - TY - JOUR AB - The adipose tissue (AT) is multifunctional, acting as an endocrine tissue and participating in the regulation of the organism's homeostasis. Metabolic, endocrine and inflammatory mechanisms are tightly intertwined within the AT, regulating its function. Disruption of the equilibrium among these mechanisms leads to pathologies, the most common being obesity-related insulin resistance. Two types of AT exist, the white and the brown AT. Traditionally the white AT (WAT) was thought to store energy in the form of lipids, while the brown AT (BAT) was known to mediate heat generation. Recently, the 'brite' or 'beige' AT was identified, which is localized predominantly in subcutaneous WAT, but shares functional features with the BAT and is capable of heat production. The major stimulus triggering beige and brown adipogenesis is cold exposure and catecholamine signalling. However, several further signals and mechanisms exist, which can orchestrate and fine-tune beige and brown AT function. Immune cells and inflammation have emerged as regulators of beige and brown AT function. The present review will focus on the recently identified crosstalk between innate immunity and the regulation of beige and brown adipogenesis. AU - Alexaki, V.I.* AU - Chavakis, T. C1 - 48865 C2 - 41457 CY - Dordrecht SP - 41-49 TI - The role of innate immunity in the regulation of brown and beige adipogenesis. JO - Rev. Endocr. Metab. Disord. VL - 17 IS - 1 PB - Springer PY - 2016 SN - 1389-9155 ER - TY - JOUR AB - In ancient Greek medicine the concept of a distinct syndrome (going together) was used to label 'a group of signs and symptoms' that occur together and 'characterize a particular abnormality and condition'. The (dys)metabolic syndrome is a common cluster of five pre-morbid metabolic-vascular risk factors or diseases associated with increased cardiovascular morbidity, fatty liver disease and risk of cancer. The risk for major complications such as cardiovascular diseases, NASH and some cancers develops along a continuum of risk factors into clinical diseases. Therefore we still include hyperglycemia, visceral obesity, dyslipidemia and hypertension as diagnostic traits in the definition according to the term 'deadly quartet'. From the beginning elevated blood pressure and hyperglycemia were core traits of the metabolic syndrome associated with endothelial dysfunction and increased risk of cardiovascular disease. Thus metabolic and vascular abnormalities are in extricable linked. Therefore it seems reasonable to extend the term to metabolic-vascular syndrome (MVS) to signal the clinical relevance and related risk of multimorbidity. This has important implications for integrated diagnostics and therapeutic approach. According to the definition of a syndrome the rapid global rise in the prevalence of all traits and comorbidities of the MVS is mainly caused by rapid changes in life-style and sociocultural transition resp. with over- and malnutrition, low physical activity and social stress as a common soil. AU - Hanefeld, M.* AU - Pistrosch, F.* AU - Bornstein, S.R. AU - Birkenfeld, A.L. C1 - 48866 C2 - 41456 CY - Dordrecht SP - 5-17 TI - The metabolic vascular syndrome - guide to an individualized treatment. JO - Rev. Endocr. Metab. Disord. VL - 17 IS - 1 PB - Springer PY - 2016 SN - 1389-9155 ER - TY - JOUR AB - The low grade inflammatory state present in obesity promotes the progression of Non-Alcoholic Fatty Liver Disease (NAFLD). In Non-Alcoholic Steatohepatitis (NASH), augmented hepatic steatosis is accompanied by aberrant intrahepatic inflammation and exacerbated hepatocellular injury. NASH is an important disorder and can lead to fibrosis, cirrhosis and even neoplasia. The pathology of NASH involves a complex network of mechanisms, including increased infiltration of different subsets of immune cells, such as monocytes, T-lymphocytes and neutrophils, to the liver, as well as activation and in situ expansion of liver resident cells such as Kupffer cells or stellate cells. In this review, we summarize recent advances regarding understanding the role of the various cells of the innate and adaptive immunity in NASH development and progression, and discuss possible future therapeutic options and tools to interfere with disease progression. AU - Nati, M.* AU - Haddad, D.* AU - Birkenfeld, A.L. AU - Koch, C.A.* AU - Chavakis, T. AU - Chatzigeorgiou, A. C1 - 48048 C2 - 39877 CY - Dordrecht SP - 29-39 TI - The role of immune cells in metabolism-related liver inflammation and development of Non-Alcoholic Steatohepatitis (NASH). JO - Rev. Endocr. Metab. Disord. VL - 17 IS - 1 PB - Springer PY - 2016 SN - 1389-9155 ER - TY - JOUR AB - Obesity, and its associated comorbidities such as type 2 diabetes, cardiovascular diseases, and certain cancers, represent major health challenges. Importantly, there is a sexual dimorphism with respect to the prevalence of obesity and its associated metabolic diseases, implicating a role for gonadal hormones. Specifically, estrogens have been demonstrated to regulate metabolism perhaps by acting as a leptin mimetic in the central nervous system (CNS). CNS estrogen receptors (ERs) include ER alpha (ERα) and ER beta (ERβ), which are found in nuclear, cytoplasmic and membrane sites throughout the brain. Additionally, estrogens can bind to and activate a G protein-coupled estrogen receptor (GPER), which is a membrane-associated ER. ERs are expressed on neurons as well as glia, which are known to play a major role in providing nutrient supply for neurons and have recently received increasing attention for their potentially important involvement in the CNS regulation of systemic metabolism and energy balance. This brief overview summarizes data focusing on the potential role of astrocytic estrogen action as a key component of estrogenic modulation responsible for mediating the sexual dimorphism in body weight regulation and obesity. AU - Fuente-Martin, E. AU - García-Cáceres, C. AU - Morselli, E.* AU - Clegg, D.J.* AU - Chowen, J.A.* AU - Finan, B. AU - Brinton, R.D.* AU - Tschöp, M.H. C1 - 27481 C2 - 32691 SP - 331-338 TI - Estrogen, astrocytes and the neuroendocrine control of metabolism. JO - Rev. Endocr. Metab. Disord. VL - 14 IS - 4 PB - Springer PY - 2013 SN - 1389-9155 ER -