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Article ; Online: Sensory spinal interoceptive pathways and energy balance regulation

Heike Münzberg / Hans-Rudolf Berthoud / Winfried L. Neuhuber

Molecular Metabolism, Vol 78, Iss , Pp 101817- (2023)

2023

Abstract: Interoception plays an important role in homeostatic regulation of energy intake and metabolism. Major interoceptive pathways include gut-to-brain and adipose tissue-to brain signaling via vagal sensory nerves and hormones, such as leptin. However, ... ...

Abstract	Interoception plays an important role in homeostatic regulation of energy intake and metabolism. Major interoceptive pathways include gut-to-brain and adipose tissue-to brain signaling via vagal sensory nerves and hormones, such as leptin. However, signaling via spinal sensory neurons is rapidly emerging as an additional important signaling pathway. Here we provide an in-depth review of the known anatomy and functions of spinal sensory pathways and discuss potential mechanisms relevant for energy balance homeostasis in health and disease. Because sensory innervation by dorsal root ganglia (DRG) neurons goes far beyond vagally innervated viscera and includes adipose tissue, skeletal muscle, and skin, it is in a position to provide much more complete metabolic information to the brain. Molecular and anatomical identification of function specific DRG neurons will be important steps in designing pharmacological and neuromodulation approaches to affect energy balance regulation in disease states such as obesity, diabetes, and cancer.
Keywords	Interoception ; Food intake ; Energy expenditure ; Obesity ; Diabetes ; Gut-brain communication ; Internal medicine ; RC31-1245
Subject code	571
Language	English
Publishing date	2023-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Regulation of body weight

Vance L. Albaugh / Yanlin He / Heike Münzberg / Christopher D. Morrison / Sangho Yu / Hans-Rudolf Berthoud

Molecular Metabolism, Vol 68, Iss , Pp 101517- (2023)

Lessons learned from bariatric surgery

2023

Abstract: Background: Bariatric or weight loss surgery is currently the most effective treatment for obesity and metabolic disease. Unlike dieting and pharmacology, its beneficial effects are sustained over decades in most patients, and mortality is among the ... ...

Abstract	Background: Bariatric or weight loss surgery is currently the most effective treatment for obesity and metabolic disease. Unlike dieting and pharmacology, its beneficial effects are sustained over decades in most patients, and mortality is among the lowest for major surgery. Because there are not nearly enough surgeons to implement bariatric surgery on a global scale, intensive research efforts have begun to identify its mechanisms of action on a molecular level in order to replace surgery with targeted behavioral or pharmacological treatments. To date, however, there is no consensus as to the critical mechanisms involved. Scope of review: The purpose of this non-systematic review is to evaluate the existing evidence for specific molecular and inter-organ signaling pathways that play major roles in bariatric surgery-induced weight loss and metabolic benefits, with a focus on Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG), in both humans and rodents. Major conclusions: Gut-brain communication and its brain targets of food intake control and energy balance regulation are complex and redundant. Although the relatively young science of bariatric surgery has generated a number of hypotheses, no clear and unique mechanism has yet emerged. It seems increasingly likely that the broad physiological and behavioral effects produced by bariatric surgery do not involve a single mechanism, but rather multiple signaling pathways. Besides a need to improve and better validate surgeries in animals, advanced techniques, including inducible, tissue-specific knockout models, and the use of humanized physiological traits will be necessary. State-of-the-art genetically-guided neural identification techniques should be used to more selectively manipulate function-specific pathways.
Keywords	Gut-brain communication ; Neural controls of food intake ; Energy balance regulation ; Gut hormones ; Bile acid signaling ; Gut microbiome ; Internal medicine ; RC31-1245
Subject code	616
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Recent advances in understanding the role of leptin in energy homeostasis [version 1; peer review

Heike Münzberg / Prachi Singh / Steven B. Heymsfield / Sangho Yu / Christopher D. Morrison

F1000Research, Vol

2 approved]

2020 Volume 9

Abstract: The hormone leptin plays a critical role in energy homeostasis, although our overall understanding of acutely changing leptin levels still needs improvement. Several developments allow a fresh look at recent and early data on leptin action. This review ... ...

Abstract	The hormone leptin plays a critical role in energy homeostasis, although our overall understanding of acutely changing leptin levels still needs improvement. Several developments allow a fresh look at recent and early data on leptin action. This review highlights select recent publications that are relevant for understanding the role played by dynamic changes in circulating leptin levels. We further discuss the relevance for our current understanding of leptin signaling in central neuronal feeding and energy expenditure circuits and highlight cohesive and discrepant findings that need to be addressed in future studies to understand how leptin couples with physiological adaptations of food intake and energy expenditure.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Targeting the T-type calcium channel Cav3.2 in GABAergic arcuate nucleus neurons to treat obesity

Bing Feng / Jerney Harms / Nirali Patel / Hui Ye / Pei Luo / Valeria Torres Irizarry / Jacob Vidrine / Ann Coulter / Candida J. Rebello / Sangho Yu / Jia Fan / Hans-Rudolf Berthoud / Frank Greenway / Heike Münzberg / Christopher Morrison / Pingwen Xu / Yanlin He

Molecular Metabolism, Vol 54, Iss , Pp 101391- (2021)

2021

Abstract: Objective: Cav3.2, a T-type low voltage-activated calcium channel widely expressed throughout the central nervous system, plays a vital role in neuronal excitability and various physiological functions. However, the effects of Cav3.2 on energy ... ...

Abstract	Objective: Cav3.2, a T-type low voltage-activated calcium channel widely expressed throughout the central nervous system, plays a vital role in neuronal excitability and various physiological functions. However, the effects of Cav3.2 on energy homeostasis remain unclear. Here, we examined the role of Cav3.2 expressed by hypothalamic GABAergic neurons in the regulation of food intake and body weight in mice and explored the underlying mechanisms. Methods: Male congenital Cana1h (the gene coding for Cav3.2) global knockout (Cav3.2KO) mice and their wild type (WT) littermates were first used for metabolic phenotyping studies. By using the CRISPR-Cas9 technique, Cav3.2 was selectively deleted from GABAergic neurons in the arcuate nucleus of the hypothalamus (ARH) by specifically overexpressing Cas9 protein and Cav3.2-targeting sgRNAs in ARH Vgat (VgatARH) neurons. These male mutants (Cav3.2KO-VgatARH) were used to determine whether Cav3.2 expressed by VgatARH neurons is required for the proper regulation of energy balance. Subsequently, we used an electrophysiological patch-clamp recording in ex vivo brain slices to explore the impact of Cav3.2KO on the cellular excitability of VgatARH neurons. Results: Male Cav3.2KO mice had significantly lower food intake than their WT littermate controls when fed with either a normal chow diet (NCD) or a high-fat diet (HFD). This hypophagia phenotype was associated with increased energy expenditure and decreased fat mass, lean mass, and total body weight. Selective deletion of Cav3.2 in VgatARH neurons resulted in similar feeding inhibition and lean phenotype without changing energy expenditure. These data provides an intrinsic mechanism to support the previous finding on ARH non-AgRP GABA neurons in regulating diet-induced obesity. Lastly, we found that naringenin extract, a predominant flavanone found in various fruits and herbs and known to act on Cav3.2, decreased the firing activity of VgatARH neurons and reduced food intake and body weight. These naringenin-induced ...
Keywords	Cav3.2 ; GABA neurons ; Feeding ; Hypothalamus ; Obesity ; Naringenin ; Internal medicine ; RC31-1245
Subject code	590
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: FGF21 is required for protein restriction to extend lifespan and improve metabolic health in male mice

Cristal M. Hill / Diana C. Albarado / Lucia G. Coco / Redin A. Spann / Md Shahjalal Khan / Emily Qualls-Creekmore / David H. Burk / Susan J. Burke / J. Jason Collier / Sangho Yu / David H. McDougal / Hans-Rudolf Berthoud / Heike Münzberg / Andrzej Bartke / Christopher D. Morrison

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 14

Abstract: The restriction of dietary protein or amino acid intake is well established to extend lifespan in multiple species. Here, the authors show that the endocrine hormone FGF21 is necessary for dietary protein restriction to extend lifespan and improve ... ...

Abstract	The restriction of dietary protein or amino acid intake is well established to extend lifespan in multiple species. Here, the authors show that the endocrine hormone FGF21 is necessary for dietary protein restriction to extend lifespan and improve metabolic health in aged, male mice.
Keywords	Science ; Q
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints

Cristal M. Hill / Thomas Laeger / Diana C. Albarado / David H. McDougal / Hans-Rudolf Berthoud / Heike Münzberg / Christopher D. Morrison

Scientific Reports, Vol 7, Iss 1, Pp 1-

2017 Volume 11

Abstract: Abstract Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of ... ...

Abstract	Abstract Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of energy expenditure during protein restriction requires UCP1, promotes a resistance to cold stress, and is dependent on the concomitant hyperphagia. Wildtype, Ucp1-KO and Fgf21-KO mice were placed on control and low protein (LP) diets to assess changes in energy expenditure, food intake and other metabolic endpoints. Deletion of Ucp1 blocked LP-induced increases in energy expenditure and food intake, and exacerbated LP-induced weight loss. While LP diet increased energy expenditure and Ucp1 expression in an FGF21-dependent manner, neither LP diet nor the deletion of Fgf21 influenced sensitivity to acute cold stress. Finally, LP-induced energy expenditure occurred even in the absence of hyperphagia. Increased energy expenditure is a primary metabolic effect of dietary protein restriction, and requires both UCP1 and FGF21 but is independent of changes in food intake. However, the FGF21-dependent increase in UCP1 and energy expenditure by LP has no effect on the ability to acutely respond to cold stress, suggesting that LP-induced increases in FGF21 impact metabolic but not thermogenic endpoints.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Gastric bypass surgery in lean adolescent mice prevents diet-induced obesity later in life

Michael B. Mumphrey / Zheng Hao / R. Leigh Townsend / Emily Qualls-Creekmore / Sangho Yu / Thomas A. Lutz / Heike Münzberg / Christopher D. Morrison / Hans-Rudolf Berthoud

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 14

Abstract: Abstract Gastric bypass surgery is the most effective treatment and is often the only option for subjects with severe obesity. However, investigation of critical molecular mechanisms involved has been hindered by confounding of specific effects of ... ...

Abstract	Abstract Gastric bypass surgery is the most effective treatment and is often the only option for subjects with severe obesity. However, investigation of critical molecular mechanisms involved has been hindered by confounding of specific effects of surgery and side effects associated with acute surgical trauma. Here, we dissociate the two components by carrying out surgery in the lean state and testing its effectiveness to prevent diet-induced obesity later in life. Body weight and composition of female mice with RYGB performed at 6 weeks of age were not significantly different from sham-operated and age-matched non-surgical mice at the time of high-fat diet exposure 12 weeks after surgery. These female mice were completely protected from high-fat diet-induced obesity and accompanying metabolic impairments for up to 50 weeks. Similar effects were seen in male mice subjected to RYGB at 5–6 weeks, although growth was slightly inhibited and protection from diet-induced obesity was less complete. The findings confirm that RYGB does not indiscriminately lower body weight but specifically prevents excessive diet-induced obesity and ensuing metabolic impairments. This prevention of obesity model should be crucial for identifying the molecular mechanisms underlying gastric bypass surgery.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2019-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Roux-en-Y gastric bypass surgery is effective in fibroblast growth factor-21 deficient mice

Christopher D. Morrison / Zheng Hao / Michael B. Mumphrey / R. Leigh Townsend / Heike Münzberg / Jianping Ye / Hans-Rudolf Berthoud

Molecular Metabolism, Vol 5, Iss 10, Pp 1006-

2016 Volume 1014

Abstract: Objective: The mechanisms by which bariatric surgeries so effectively and lastingly reduce body weight and normalize metabolic dysfunction are not well understood. Fibroblast growth fator-21 (FGF21) is a key regulator of metabolism and is currently ... ...

Abstract	Objective: The mechanisms by which bariatric surgeries so effectively and lastingly reduce body weight and normalize metabolic dysfunction are not well understood. Fibroblast growth fator-21 (FGF21) is a key regulator of metabolism and is currently considered for treatment of obesity. Although elevated by acute food deprivation, it is downregulated after weight loss induced by chronic calorie restriction but not after Roux-en-Y gastric bypass surgery. Therefore, the goal of the present study was to assess the role of FGF21-signaling in the beneficial effects of Roux-en-Y gastric bypass surgery (RYGB). Methods: High-fat diet-induced obese FGF21-deficient (FGF21−/−) and wildtype (WT) mice were subjected to RYGB, sham surgery, or caloric restriction to match body weight of RYGB mice. Body weight, body composition, food intake, energy expenditure, glucose tolerance, and insulin sensitivity, as well as plasma levels and hepatic mRNA expression of FGF21 were measured. Results: Hepatic expression and plasma levels of FGF21 are higher after RYGB compared with similar weight loss induced by caloric restriction, suggesting that elevated FGF21 might play a role in preventing increased hunger and weight regain after RYGB. However, although the body weight differential between RYGB and sham surgery was significantly reduced in FGF21−/− mice, RYGB induced similarly sustained body weight and fat mass loss, initial reduction of food intake, increased energy expenditure, and improvements in glycemic control in FGF21−/− and WT mice. Conclusions: FGF21 signaling is not a critical single factor for the beneficial metabolic effects of RYGB. This may open up the possibility to use FGF21 as adjuvant therapy in patients with ineffective bariatric surgeries. Keywords: Obesity, Diabetes, Body weight, Food intake, Energy expenditure, Glucose tolerance, Insulin, Leptin
Keywords	Internal medicine ; RC31-1245
Subject code	630
Language	English
Publishing date	2016-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Galanin neurons in the ventrolateral preoptic area promote sleep and heat loss in mice

Daniel Kroeger / Gianna Absi / Celia Gagliardi / Sathyajit S. Bandaru / Joseph C. Madara / Loris L. Ferrari / Elda Arrigoni / Heike Münzberg / Thomas E. Scammell / Clifford B. Saper / Ramalingam Vetrivelan

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 14

Abstract: Anatomical lesions of the preoptic area (POA) can cause sleep loss while electrical, chemical, or thermal stimulation of POA can induce sleep. To better understand the exact neural function of the POA, this study shows that galanin and GABA+ inhibitory ... ...

Abstract	Anatomical lesions of the preoptic area (POA) can cause sleep loss while electrical, chemical, or thermal stimulation of POA can induce sleep. To better understand the exact neural function of the POA, this study shows that galanin and GABA+ inhibitory neurons in the ventrolateral POA that project to the wake-promoting tuberomammillary nucleus promote sleep in a stimulation frequency dependent manner.
Keywords	Science ; Q
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Galanin neurons in the ventrolateral preoptic area promote sleep and heat loss in mice

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 14

Abstract	Anatomical lesions of the preoptic area (POA) can cause sleep loss while electrical, chemical, or thermal stimulation of POA can induce sleep. To better understand the exact neural function of the POA, this study shows that galanin and GABA+ inhibitory neurons in the ventrolateral POA that project to the wake-promoting tuberomammillary nucleus promote sleep in a stimulation frequency dependent manner.
Keywords	Science ; Q
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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