Eric D. Berglund

The University of Texas Southwestern Medical Center

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Joel K. Elmquist

The University of Texas Southwestern Medical Center

David H. Wasserman

Vanderbilt University

Tiemin Liu

Zhongshan Hospital

Charlotte E. Lee

University of Stirling

Kevin W. Williams

The University of Texas Southwestern Medical Center

Cláudia R. Vianna

The University of Texas Southwestern Medical Center

Chen Liu

The University of Texas Southwestern Medical Center

Jeffrey M. Zigman

The University of Texas Southwestern Medical Center

Maureen Charron

Albert Einstein College of Medicine

Sara E. Lynes

Vanderbilt University

Cooperative Institutions

The University of Texas Southwestern Medical Center

124

Southwestern Medical Center

Harvard University

Vanderbilt University

University of Michigan–Ann Arbor

Baylor College of Medicine

Howard Hughes Medical Institute

Advanced Imaging Research (United States)

The University of Texas Health Science Center at Houston

Stanford University

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The starvation hormone, fibroblast growth factor-21, extends lifespan in mice

eLife (2012)

Yuan Zhang Yang Xie Eric D. Berglund Katie C. Coate Tian He

Fibroblast growth factor-21 (FGF21) is a hormone secreted by the liver during fasting that elicits diverse aspects of the adaptive starvation response. Among its effects, FGF21 induces hepatic fatty acid oxidation and ketogenesis, increases insulin sensitivity, blocks somatic growth and causes bone loss. Here we show that transgenic overexpression of FGF21 markedly extends lifespan in mice without reducing food intake or affecting markers of NAD+ metabolism or AMP kinase and mTOR signaling. Transcriptomic analysis suggests that FGF21 acts primarily by blunting the growth hormone/insulin-like growth factor-1 signaling pathway in liver. These findings raise the possibility that FGF21 can be used to extend lifespan in other species.

FGF21

Ketogenesis

10.7554/elife.00065

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Citations (375)

Hepatic Glucagon Action Is Essential for Exercise-Induced Reversal of Mouse Fatty Liver

Diabetes (2011)

Eric D. Berglund Daniel G. Lustig Richard A. Baheza Clinton M. Hasenour Robert S. Lee

Exercise is an effective intervention to treat fatty liver. However, the mechanism(s) that underlie exercise-induced reductions in fatty liver are unclear. Here we tested the hypothesis that exercise requires hepatic glucagon action to reduce fatty liver.C57BL/6 mice were fed high-fat diet (HFD) and assessed using magnetic resonance, biochemical, and histological techniques to establish a timeline for fatty liver development over 20 weeks. Glucagon receptor null (gcgr(-/-)) and wild-type (gcgr(+/+)) littermate mice were subsequently fed HFD to provoke moderate fatty liver and then performed either 10 or 6 weeks of running wheel or treadmill exercise, respectively.Exercise reverses progression of HFD-induced fatty liver in gcgr(+/+) mice. Remarkably, such changes are absent in gcgr(-/-) mice, thus confirming the hypothesis that exercise-stimulated hepatic glucagon receptor activation is critical to reduce HFD-induced fatty liver.These findings suggest that therapies that use antagonism of hepatic glucagon action to reduce blood glucose may interfere with the ability of exercise and perhaps other interventions to positively affect fatty liver.

Glucagon receptor

10.2337/db11-0455

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Citations (41)

Emerging role of AMP-activated protein kinase in endocrine control of metabolism in the liver

Molecular and Cellular Endocrinology (2012)

Clinton M. Hasenour Eric D. Berglund David H. Wasserman

AMP-Activated Protein Kinase

10.1016/j.mce.2012.06.018

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Citations (87)

Pulmonary gas exchange at rest and during exercise in chronic bronchitis.

PubMed (1971)

Simonsson Bg R Malmberg Eric D. Berglund

Rest (music)

Chronic bronchitis

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Fibroblast Growth Factor 21 Controls Glycemia via Regulation of Hepatic Glucose Flux and Insulin Sensitivity

Endocrinology (2009)

Eric D. Berglund Candice Y. Li Holly A. Bina Sara E. Lynes M. Dodson Michael

Abstract Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator shown to improve glycemic control. However, the molecular and functional mechanisms underlying FGF21-mediated improvements in glycemic control are not completely understood. We examined FGF21 effects on insulin sensitivity and glucose fluxes upon chronic (daily injection for 8 d) and acute (6 h infusion) administration in ob/+ and ob/ob mice. Results show that chronic FGF21 ameliorated fasting hyperglycemia in ob/ob mice via increased glucose disposal and improved hepatic insulin sensitivity. Acute FGF21 suppressed hepatic glucose production, increased liver glycogen, lowered glucagon, and improved glucose clearance in ob/+ mice. These effects were blunted in ob/ob mice. Neither chronic nor acute FGF21 altered skeletal muscle or adipose tissue glucose uptake in either genotype. In conclusion, FGF21 has potent glycemic effects caused by hepatic changes in glucose flux and improved insulin sensitivity. Thus, these studies define mechanisms underlying anti-hyperglycemic actions of FGF21 and support its therapeutic potential.

FGF21

Carbohydrate Metabolism

Glucose clamp technique

10.1210/en.2009-0221

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Citations (277)

Observations on obstructive lung disease in Scandinavia

Tubercle (1975)

Eric D. Berglund

Obstructive lung disease

10.1016/0041-3879(75)90035-5

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Citations (0)

Direct Insulin and Leptin Action on Pro-opiomelanocortin Neurons Is Required for Normal Glucose Homeostasis and Fertility

Cell Metabolism (2010)

Jennifer W. Hill Carol F. Elias Makoto Fukuda Kevin W. Williams Eric D. Berglund

Energy homeostasis

Leptin receptor

Homeostasis

10.1016/j.cmet.2010.03.002

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Citations (366)

Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis (Journal of Clinical Investigation (2014) 124, 4 (1868) DOI: 10.1172/JCI75669)

Journal of Clinical Investigation (2014)

Eric D. Berglund Chen Liu Jong Woo Sohn Tiemin Liu Mi Hwa Kim

Homeostasis

Energy homeostasis

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Action of Neurotransmitter: A Key to Unlock the AgRP Neuron Feeding Circuit

Frontiers in Neuroscience (2013)

Tiemin Liu Qian Wang Eric D. Berglund Qingchun Tong

The current obesity epidemic and lack of efficient therapeutics demand a clear understanding of the mechanism underlying body weight regulation. Despite intensive research focus on obesity pathogenesis, an effective therapeutic strategy to treat and cure obesity is still lacking. Exciting studies in last decades have established the importance of hypothalamic agouti-related protein-expressing neurons (AgRP neurons) in the regulation of body weight homeostasis. AgRP neurons are both required and sufficient for feeding regulation. The activity of AgRP neurons is intricately regulated by nutritional hormones as well as synaptic inputs from upstream neurons. Changes in AgRP neuron activity lead to alterations in the release of mediators, including neuropeptides Neuropeptide Y (NPY) and AgRP, and fast-acting neurotransmitter GABA. Recent studies based on mouse genetics, novel optogenetics, and designer receptor exclusively activated by designer drugs have identified a critical role for GABA release from AgRP neurons in the parabrachial nucleus and paraventricular hypothalamus in feeding control. This review will summarize recent findings about AgRP neuron-mediated control of feeding circuits with a focus on the role of neurotransmitters. Given the limited knowledge on feeding regulation, understanding the action of neurotransmitters may be a key to unlock neurocircuitry that governs feeding.

Neurotransmitter Agents

10.3389/fnins.2012.00200

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Citations (29)

Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis

Journal of Clinical Investigation (2013)

Eric D. Berglund Chen Liu Jong-Woo Sohn Tiemin Liu Mi Hwa Kim

Energy and glucose homeostasis are regulated by central serotonin 2C receptors. These receptors are attractive pharmacological targets for the treatment of obesity; however, the identity of the serotonin 2C receptor-expressing neurons that mediate the effects of serotonin and serotonin 2C receptor agonists on energy and glucose homeostasis are unknown. Here, we show that mice lacking serotonin 2C receptors (Htr2c) specifically in pro-opiomelanocortin (POMC) neurons had normal body weight but developed glucoregulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, and insulin resistance. Moreover, these mice did not show anorectic responses to serotonergic agents that suppress appetite and developed hyperphagia and obesity when they were fed a high-fat/high-sugar diet. A requirement of serotonin 2C receptors in POMC neurons for the maintenance of normal energy and glucose homeostasis was further demonstrated when Htr2c loss was induced in POMC neurons in adult mice using a tamoxifen-inducible POMC-cre system. These data demonstrate that serotonin 2C receptor-expressing POMC neurons are required to control energy and glucose homeostasis and implicate POMC neurons as the target for the effect of serotonin 2C receptor agonists on weight-loss induction and improved glycemic control.

Energy homeostasis

Hyperinsulinemia

Homeostasis

10.1172/jci70338

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Citations (207)