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Article ; Online: Maternal Metabolic Programming of the Developing Central Nervous System: Unified Pathways to Metabolic and Psychiatric Disorders.

Lippert, Rachel N / Brüning, Jens C

2021 Volume 91, Issue 10, Page(s) 898–906

Abstract: The perinatal period presents a critical time in offspring development where environmental insults can have damaging impacts on the future health of the offspring. This can lead to sustained alterations in offspring development, metabolism, and ... ...

Abstract	The perinatal period presents a critical time in offspring development where environmental insults can have damaging impacts on the future health of the offspring. This can lead to sustained alterations in offspring development, metabolism, and predisposition to both metabolic and psychiatric diseases. The central nervous system is one of the most sensitive targets in response to maternal obesity and/or type 2 diabetes mellitus. While many of the effects of obesity on brain function in adults are known, we are only now beginning to understand the multitude of changes that occur in the brain during development on exposure to maternal overnutrition. Specifically, given recent links between maternal metabolic state and onset of neurodevelopmental diseases, the specific changes that are occurring in the offspring are even more relevant for the study of disease onset. It is therefore critical to understand the developmental effects of maternal obesity and/or type 2 diabetes mellitus and further to define the underlying cellular and molecular changes in the fetal brain. This review focuses on the current advancements in the study of maternal programming of brain development with particular emphasis on brain connectivity, specific regional effects, newly studied peripheral contributors, and key windows of interventions where maternal bodyweight and food intake may drive the most detrimental effects on the brain and associated metabolic and behavioral consequences.
MeSH term(s)	Adult ; Brain ; Diabetes Mellitus, Type 2 ; Female ; Humans ; Neurodevelopmental Disorders/etiology ; Obesity, Maternal ; Pregnancy ; Prenatal Exposure Delayed Effects
Language	English
Publishing date	2021-06-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2021.06.002
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Article ; Online: Gut-derived peptide hormone receptor expression in the developing mouse hypothalamus.

Cantacorps, Lídia / Coull, Bethany M / Falck, Joanne / Ritter, Katrin / Lippert, Rachel N

PloS one

2023 Volume 18, Issue 8, Page(s) e0290043

Abstract: Objective: In adult organisms, a number of receptors have been identified which modulate metabolic processes related to peptides derived from the intestinal tract. These receptors play significant roles in glucose homeostasis, food intake and energy ... ...

Abstract	Objective: In adult organisms, a number of receptors have been identified which modulate metabolic processes related to peptides derived from the intestinal tract. These receptors play significant roles in glucose homeostasis, food intake and energy balance. Here we assess these classical metabolic receptors and their expression as well as their potential role in early development of hypothalamic neuronal circuits. Methods: Chow-fed C57BL6/N female mice were mated and hypothalamic tissue was collected from offspring across postnatal development (postnatal day 7-21). Subsequent qPCR and Western Blot analyses were used to determine mRNA and protein changes in gut-derived peptide hormone receptors. Correlations to body weight, blood glucose and circulating leptin levels were analyzed. Results: We describe the gene expression and dynamic protein regulation of key gut-derived peptide hormone receptors in the early postnatal period of the mouse brain. Specifically, we show changes to Gastric inhibitory polypeptide receptor (GIPR), glucagon-like peptide 1 receptor (GLP1R), and cholecystokinin receptor 2 (CCK2R) in the developing hypothalamus. The changes to GIPR and InsR seem to be strongly negatively correlated with body weight. Conclusions: This comprehensive analysis underscores the need to understand the roles of maternal-derived circulating gut hormones and their direct effect on offspring brain development.
MeSH term(s)	Female ; Animals ; Mice ; Receptors, Peptide ; Blood Glucose ; Blotting, Western ; Body Weight ; Brain
Chemical Substances	Receptors, Peptide ; Blood Glucose
Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0290043
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Article ; Online: Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior.

Igual Gil, Carla / Coull, Bethany M / Jonas, Wenke / Lippert, Rachel N / Klaus, Susanne / Ost, Mario

Life science alliance

2022 Volume 5, Issue 11

Abstract: Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate ... ...

Abstract	Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate endocrine GDF15 signaling to the brain upon mitochondrial dysfunction is still unknown. Using a mouse model with muscle-specific mitochondrial dysfunction, we here show that GFRAL is required for activation of systemic energy metabolism via daytime-restricted anorexia but not responsible for muscle wasting. We further find that muscle mitochondrial stress response involves a GFRAL-dependent induction of hypothalamic corticotropin-releasing hormone, without elevated corticosterone levels. Finally, we identify that GFRAL signaling governs an anxiety-like behavior in male mice with muscle mitochondrial dysfunction, with females showing a less robust GFRAL-dependent anxiety-like phenotype. Together, we here provide novel evidence of a mitochondrial stress-induced muscle-brain crosstalk via the GDF15-GFRAL axis to modulate food intake and anxiogenic behavior.
MeSH term(s)	Female ; Male ; Humans ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Growth Differentiation Factor 15/pharmacology ; Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism ; Obesity/metabolism ; Corticotropin-Releasing Hormone ; Corticosterone ; Glial Cell Line-Derived Neurotrophic Factor ; Eating/genetics ; Anxiety
Chemical Substances	Growth Differentiation Factor 15 ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Corticotropin-Releasing Hormone (9015-71-8) ; Corticosterone (W980KJ009P) ; Glial Cell Line-Derived Neurotrophic Factor
Language	English
Publishing date	2022-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201495
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Article ; Online: Organization of neural systems expressing melanocortin-3 receptors in the mouse brain: Evidence for sexual dimorphism.

Bedenbaugh, Michelle N / Brener, Samantha C / Maldonado, Jose / Lippert, Rachel N / Sweeney, Patrick / Cone, Roger D / Simerly, Richard B

The Journal of comparative neurology

2022 Volume 530, Issue 16, Page(s) 2835–2851

Abstract: The central melanocortin system is fundamentally important for controlling food intake and energy homeostasis. Melanocortin-3 receptor (MC3R) is one of two major receptors of the melanocortin system found in the brain. In contrast to the well- ... ...

Abstract	The central melanocortin system is fundamentally important for controlling food intake and energy homeostasis. Melanocortin-3 receptor (MC3R) is one of two major receptors of the melanocortin system found in the brain. In contrast to the well-characterized melanocortin-4 receptor (MC4R), little is known regarding the organization of MC3R-expressing neural circuits. To increase our understanding of the intrinsic organization of MC3R neural circuits, identify specific differences between males and females, and gain a neural systems level perspective of this circuitry, we conducted a brain-wide mapping of neurons labeled for MC3R and characterized the distribution of their projections. Analysis revealed MC3R neuronal and terminal labeling in multiple brain regions that control a diverse range of physiological functions and behavioral processes. Notably, dense labeling was observed in the hypothalamus, as well as areas that share considerable connections with the hypothalamus, including the cortex, amygdala, thalamus, and brainstem. Additionally, MC3R neuronal labeling was sexually dimorphic in several areas, including the anteroventral periventricular area, arcuate nucleus, principal nucleus of the bed nucleus of the stria terminalis, and ventral premammillary region. Altogether, anatomical evidence reported here suggests that MC3R has the potential to influence several different classes of motivated behavior that are essential for survival, including ingestive, reproductive, defensive, and arousal behaviors, and is likely to modulate these behaviors differently in males and females.
MeSH term(s)	Animals ; Brain/metabolism ; Female ; Hypothalamus/metabolism ; Male ; Melanocortins ; Mice ; Receptor, Melanocortin, Type 3/genetics ; Receptor, Melanocortin, Type 3/metabolism ; Sex Characteristics
Chemical Substances	Mc3r protein, mouse ; Melanocortins ; Receptor, Melanocortin, Type 3
Language	English
Publishing date	2022-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.25379
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Article ; Online: Developmental metformin exposure does not rescue physiological impairments derived from early exposure to altered maternal metabolic state in offspring mice.

Cantacorps, Lídia / Zhu, Jiajie / Yagoub, Selma / Coull, Bethany M / Falck, Joanne / Chesters, Robert A / Ritter, Katrin / Serrano-Lope, Miguel / Tscherepentschuk, Katharina / Kasch, Lea-Sophie / Paterson, Maya / Täger, Paula / Baidoe-Ansah, David / Pandey, Shuchita / Igual-Gil, Carla / Braune, Annett / Lippert, Rachel N

Molecular metabolism

2023 Volume 79, Page(s) 101860

Abstract: Objective: The incidence of gestational diabetes mellitus (GDM) and metabolic disorders during pregnancy are increasing globally. This has resulted in increased use of therapeutic interventions such as metformin to aid in glycemic control during ... ...

Abstract	Objective: The incidence of gestational diabetes mellitus (GDM) and metabolic disorders during pregnancy are increasing globally. This has resulted in increased use of therapeutic interventions such as metformin to aid in glycemic control during pregnancy. Even though metformin can cross the placental barrier, its impact on offspring brain development remains poorly understood. As metformin promotes AMPK signaling, which plays a key role in axonal growth during development, we hypothesized that it may have an impact on hypothalamic signaling and the formation of neuronal projections in the hypothalamus, the key regulator of energy homeostasis. We further hypothesized that this is dependent on the metabolic and nutritional status of the mother at the time of metformin intervention. Using mouse models of maternal overnutrition, we aimed to assess the effects of metformin exposure on offspring physiology and hypothalamic neuronal circuits during key periods of development. Methods: Female C57BL/6N mice received either a control diet or a high-fat diet (HFD) during pregnancy and lactation periods. A subset of dams was fed a HFD exclusively during the lactation. Anti-diabetic treatments were given during the first postnatal weeks. Body weights of male and female offspring were monitored daily until weaning. Circulating metabolic factors and molecular changes in the hypothalamus were assessed at postnatal day 16 using ELISA and Western Blot, respectively. Hypothalamic innervation was assessed by immunostaining at postnatal days 16 and 21. Results: We identified alterations in weight gain and circulating hormones in male and female offspring induced by anti-diabetic treatment during the early postnatal period, which were critically dependent on the maternal metabolic state. Furthermore, hypothalamic agouti-related peptide (AgRP) and proopiomelanocortin (POMC) neuronal innervation outcomes in response to anti-diabetic treatment were also modulated by maternal metabolic state. We also identified sex-specific changes in hypothalamic AMPK signaling in response to metformin exposure. Conclusion: We demonstrate a unique interaction between anti-diabetic treatment and maternal metabolic state, resulting in sex-specific effects on offspring brain development and physiological outcomes. Overall, based on our findings, no positive effect of metformin intervention was observed in the offspring, despite ameliorating effects on maternal metabolic outcomes. In fact, the metabolic state of the mother drives the most dramatic differences in offspring physiology and metformin had no rescuing effect. Our results therefore highlight the need for a deeper understanding of how maternal metabolic state (excessive weight gain versus stable weight during GDM treatment) affects the developing offspring. Further, these results emphasize that the interventions to treat alterations in maternal metabolism during pregnancy need to be reassessed from the perspective of the offspring physiology.
MeSH term(s)	Humans ; Mice ; Female ; Pregnancy ; Animals ; Male ; AMP-Activated Protein Kinases ; Placenta ; Mice, Inbred C57BL ; Weight Gain ; Diet, High-Fat/adverse effects ; Diabetes, Gestational/drug therapy
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2023-12-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101860
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Article ; Online: Gender-specific roles for the melanocortin-3 receptor in the regulation of the mesolimbic dopamine system in mice.

Lippert, Rachel N / Ellacott, Kate L J / Cone, Roger D

Endocrinology

2014 Volume 155, Issue 5, Page(s) 1718–1727

Abstract: The melanocortin-3 receptor (MC3R) and MC4R are known to play critical roles in energy homeostasis. However, the physiological functions of the MC3R remain poorly understood. Earlier reports indicated that the ventral tegmental area (VTA) is one of the ... ...

Abstract	The melanocortin-3 receptor (MC3R) and MC4R are known to play critical roles in energy homeostasis. However, the physiological functions of the MC3R remain poorly understood. Earlier reports indicated that the ventral tegmental area (VTA) is one of the highest sites of MC3R expression, and we sought to determine the function of the receptor in this brain region. A MC3R-green-fluorescent protein transgenic mouse and a MC3R knockout mouse strain were used to characterize the neurochemical identity of the MC3R neurons in the VTA and to determine the effects of global MC3R deletion on VTA dopamine (DA) homeostasis. We demonstrate that the MC3R, but not MC4R, is expressed in up to a third of dopaminergic neurons of the VTA. Global deletion of the MC3R increases total dopamine by 42% in the VTA and decreases sucrose intake and preference in female but not male mice. Ovariectomy restores dopamine levels to normal, but aberrant decreased VTA dopamine levels are also observed in prepubertal female mice. Because arcuate Agouti-related peptide/neuropeptide Y neurons are known to innervate and regulate VTA signaling, the MC3R in dopaminergic neurons provides a specific input for communication of nutritional state within the mesolimbic dopamine system. Data provided here suggest that this input may be highly sexually dimorphic, functioning as a specific circuit regulating effects of estrogen on VTA dopamine levels and on sucrose preference. Overall, this data support a sexually dimorphic function of MC3R in regulation of the mesolimbic dopaminergic system and reward.
MeSH term(s)	Animals ; Appetitive Behavior ; Behavior, Animal ; Dopamine/metabolism ; Dopaminergic Neurons/cytology ; Dopaminergic Neurons/metabolism ; Female ; Food Preferences ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Homeostasis ; Limbic System/cytology ; Limbic System/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Ovariectomy ; Promoter Regions, Genetic ; Receptor, Melanocortin, Type 3/genetics ; Receptor, Melanocortin, Type 3/metabolism ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Sex Characteristics ; Ventral Tegmental Area/cytology ; Ventral Tegmental Area/metabolism
Chemical Substances	MC4R protein, mouse ; Mc3r protein, mouse ; Nerve Tissue Proteins ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Green Fluorescent Proteins (147336-22-9) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2014-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2013-2049
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Article ; Online: Regulation of energy rheostasis by the melanocortin-3 receptor.

Ghamari-Langroudi, Masoud / Cakir, Isin / Lippert, Rachel N / Sweeney, Patrick / Litt, Michael J / Ellacott, Kate L J / Cone, Roger D

Science advances

2018 Volume 4, Issue 8, Page(s) eaat0866

Abstract: Like most homeostatic systems, adiposity in mammals is defended between upper and lower boundary conditions. While leptin and melanocortin-4 receptor (MC4R) signaling are required for defending energy set point, mechanisms controlling upper and lower ... ...

Abstract	Like most homeostatic systems, adiposity in mammals is defended between upper and lower boundary conditions. While leptin and melanocortin-4 receptor (MC4R) signaling are required for defending energy set point, mechanisms controlling upper and lower homeostatic boundaries are less well understood. In contrast to the MC4R, deletion of the MC3R does not produce measurable hyperphagia or hypometabolism under normal conditions. However, we demonstrate that MC3R is required bidirectionally for controlling responses to external homeostatic challenges, such as caloric restriction or calorie-rich diet. MC3R is also required for regulated excursion from set point, or rheostasis, during pregnancy. Further, we demonstrate a molecular mechanism: MC3R provides regulatory inputs to melanocortin signaling, acting presynaptically on agouti-related protein neurons to regulate γ-aminobutyric acid release onto anorexigenic MC4R neurons, exerting boundary control on the activity of MC4R neurons. Thus, the MC3R is a critical regulator of boundary controls on melanocortin signaling, providing rheostatic control on energy storage.
MeSH term(s)	Animals ; Energy Metabolism ; Feeding Behavior ; Female ; Homeostasis ; Inhibitory Postsynaptic Potentials/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/physiology ; Receptor, Melanocortin, Type 3/physiology
Chemical Substances	Mc3r protein, mouse ; Receptor, Melanocortin, Type 3
Language	English
Publishing date	2018-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aat0866
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Article ; Online: Time-dependent assessment of stimulus-evoked regional dopamine release.

Lippert, Rachel N / Cremer, Anna Lena / Edwin Thanarajah, Sharmili / Korn, Clio / Jahans-Price, Thomas / Burgeno, Lauren M / Tittgemeyer, Marc / Brüning, Jens C / Walton, Mark E / Backes, Heiko

Nature communications

2019 Volume 10, Issue 1, Page(s) 336

Abstract: To date, the spatiotemporal release of specific neurotransmitters at physiological levels in the human brain cannot be detected. Here, we present a method that relates minute-by-minute fluctuations of the positron emission tomography (PET) radioligand [ ... ...

Abstract	To date, the spatiotemporal release of specific neurotransmitters at physiological levels in the human brain cannot be detected. Here, we present a method that relates minute-by-minute fluctuations of the positron emission tomography (PET) radioligand [11C]raclopride directly to subsecond dopamine release events. We show theoretically that synaptic dopamine release induces low frequency temporal variations of extrasynaptic extracellular dopamine levels, at time scales of one minute, that can evoke detectable temporal variations in the [11C]raclopride signal. Hence, dopaminergic activity can be monitored via temporal fluctuations in the [11C]raclopride PET signal. We validate this theory using fast-scan cyclic voltammetry and [11C]raclopride PET in mice during chemogenetic activation of dopaminergic neurons. We then apply the method to data from human subjects given a palatable milkshake and discover immediate and-for the first time-delayed food-induced dopamine release. This method enables time-dependent regional monitoring of stimulus-evoked dopamine release at physiological levels.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/surgery ; Dopamine/metabolism ; Eating ; Electric Stimulation ; Electrodes ; Female ; Humans ; Male ; Mice ; Models, Biological ; Neurons/metabolism ; Positron-Emission Tomography/methods ; Raclopride/metabolism ; Radioligand Assay ; Temporal Lobe/metabolism ; Temporal Lobe/surgery ; Time Factors
Chemical Substances	Raclopride (430K3SOZ7G) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2019-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-08143-4
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Article ; Online: Food Intake Recruits Orosensory and Post-ingestive Dopaminergic Circuits to Affect Eating Desire in Humans.

Thanarajah, Sharmili Edwin / Backes, Heiko / DiFeliceantonio, Alexandra G / Albus, Kerstin / Cremer, Anna Lena / Hanssen, Ruth / Lippert, Rachel N / Cornely, Oliver A / Small, Dana M / Brüning, Jens C / Tittgemeyer, Marc

Cell metabolism

2018 Volume 29, Issue 3, Page(s) 695–706.e4

Abstract: Pleasant taste and nutritional value guide food selection behavior. Here, orosensory features of food may be secondary to its nutritional value in underlying reinforcement, but it is unclear how the brain encodes the reward value of food. Orosensory and ... ...

Abstract	Pleasant taste and nutritional value guide food selection behavior. Here, orosensory features of food may be secondary to its nutritional value in underlying reinforcement, but it is unclear how the brain encodes the reward value of food. Orosensory and peripheral physiological signals may act together on dopaminergic circuits to drive food intake. We combined fMRI and a novel [11C]raclopride PET method to assess systems-level activation and dopamine release in response to palatable food intake in humans. We identified immediate orosensory and delayed post-ingestive dopamine release. Both responses recruit segregated brain regions: specialized integrative pathways and higher cognitive centers. Furthermore, we identified brain areas where dopamine release reflected the subjective desire to eat. Immediate dopamine release in these wanting-related regions was inversely correlated with, and presumably inhibited, post-ingestive release in the dorsal striatum. Our results highlight the role of brain and periphery in interacting to reinforce food intake in humans.
MeSH term(s)	Adult ; Aged ; Brain/metabolism ; Dopamine/metabolism ; Eating/physiology ; Food Preferences/physiology ; Healthy Volunteers ; Humans ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Taste/physiology
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2018-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2018.12.006
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Article: Evidence for a novel functional role of astrocytes in the acute homeostatic response to high-fat diet intake in mice.

Buckman, Laura B / Thompson, Misty M / Lippert, Rachel N / Blackwell, Timothy S / Yull, Fiona E / Ellacott, Kate L J

Molecular metabolism

2015 Volume 4, Issue 1, Page(s) 58–63

Abstract: Objective: Introduction of a high-fat diet to mice results in a period of voracious feeding, known as hyperphagia, before homeostatic mechanisms prevail to restore energy intake to an isocaloric level. Acute high-fat diet hyperphagia induces astrocyte ... ...

Abstract	Objective: Introduction of a high-fat diet to mice results in a period of voracious feeding, known as hyperphagia, before homeostatic mechanisms prevail to restore energy intake to an isocaloric level. Acute high-fat diet hyperphagia induces astrocyte activation in the rodent hypothalamus, suggesting a potential role of these cells in the homeostatic response to the diet. The objective of this study was to determine physiologic role of astrocytes in the acute homeostatic response to high-fat feeding. Methods: We bred a transgenic mouse model with doxycycline-inducible inhibition of NFkappaB (NFκB) signaling in astrocytes to determine the effect of loss of NFκB-mediated astrocyte activation on acute high-fat hyperphagia. ELISA was used to measure the levels of markers of astrocyte activation, glial-fibrillary acidic protein (GFAP) and S100B, in the medial basal hypothalamus. Results: Inhibition of NFκB signaling in astrocytes prevented acute high-fat diet-induced astrocyte activation and resulted in a 15% increase in caloric intake (P < 0.01) in the first 24 h after introduction of the diet. Conclusions: These data reveal a novel homeostatic role for astrocytes in the acute physiologic regulation of food intake in response to high-fat feeding.
Language	English
Publishing date	2015-01
Publishing country	Germany
Document type	Journal Article
ISSN	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2014.10.001
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