Karolina Skibicka Group
Short description
Karolina Skibicka, PhD, Senior Lecturer (Associate Professor) in Physiology.
About Skibicka Group
Karolina Skibicka investigates the behavioral and neuroendocrine processes that govern fundamental homeostatic and reward controls of food intake, and ultimately how these systems fail in obesity. She aims to identify a more effective obesity treatment targeting the neural circuits underlying overeating.
By integrating careful experimental decomposition of behavior with neuropharmacology, genetic manipulations, and molecular methods her group aims to gain insight into how food and feeding behavior affects the brain, and in turn how the brain regulates feeding and food choices.
Recent discoveries by her group include findings that satiety or hunger hormones, for example glucagon-like peptide 1 or ghrelin, which are altered by nutritional status, affect far more than feeding behavior and body weight. They profoundly affect reward derived from food but also alcohol, emotionality and decision-making. This impact on behavior is paralleled by neurochemical and molecular changes in brain circuits regulating them.
Karolina is a strong advocate for inclusion of females in preclinical research. Males and females, humans and rodents alike, may detect and respond to signals controlling eating differently. Understanding these differences may be crucial to finding new effective anti-obesity treatments and ignoring them likely already led to discarding treatments that may have been effective in women but were without much effect in men.
International Collaborations
Karolina Skibicka has extensive international collaborations, which include researchers from University of Pennsylvania, University of Southern California, Cambridge University, University of Freiburg, and Karolinska Institute, in additional to multiple active local collaborative project.
Karolina Skibicka was appointed a Ragnar Söderberg Fellow in Medicine 2015. She has also recently been awarded the Fernström Prize in Medicine 2016 for young investigators.
Research Opportunities in the Laboratory
We welcome motivated students interested in summer internships/masters thesis projects/ other laboratory research opportunities. For more information please contact Karolina.Skibicka@gu.se
Contact Information
Karolina Skibicka
Department of Physiology
Box 432
405 30 Göteborg
Visiting Address:
Medicinaregatan 11-13,
413 90 Gothenburg
Jean-Philippe Krieger
Post-doctoral Fellow
jean-philippe.krieger@gu.se
Ph.D. in Neurophysiology, ETH Zurich (Switzerland)
M.Sc. in Nutrition Science, AgroParisTech (France)
Francesco Longo
Post-doctoral Fellow
francesco.longo@gu.se
Post-doctoral Fellow, Center for Neural Science, New York University, New York, NY, USA
Ph.D. Molecular Pharmacology and Oncology, University of Ferrara, National Institute of Neuroscience, Ferrara, Italy
M.Sc. Medicinal Chemistry and Pharmaceutical Technology, University of Ferrara, Ferrara, Italy
Jennifer Richard
Post-doctoral Fellow
jennifer.richard@gu.se
Ph.D. Medical Science: Neuroscience. University of Gothenburg, Gothenburg, Sweden. 2020
M.Sc. Pharmacology, University of Gothenburg
B.Sc. Pharmacology, University of Gothenburg
Mohammed Asker
PhD Student, Medical Science: Neuroscience.
mohammed.asker@gu.se
M.Sc. in Biomarkers in Molecular Medicine, University of Skövde, Sweden
B.Sc. in Pharmaceutical Sciences, University of Tanta, Egypt
Stina Börchers
PhD Student, Medical Science: Neuroscience.
stina.borchers@gu.se
B.Sc. Biology, University of Bremen, Germany
M.Sc. Neurosciences, University of Bremen, Germany
Ivana Maric
PhD Student, Medical Science: Neuroscience.
ivana.maric@gu.se
M.Sc. Pharmacology, University of Gothenburg
B.Sc. Pharmacology, University of Gothenburg
Pauline van der Velden
Internship researcher, M.Sc. Biology, Utrecht University, the Netherlands
pauline.van.der.velden@gu.se
B.Sc. Biomedical Sciences, Utrecht University, the Netherlands, 2018
Research Summary
The answer to tackling the obesity epidemic is in the brain
Rates of obesity are growing rapidly and there is a great need for new effective treatments. Understanding the brain mechanisms that govern how much and when we eat is key to finding solutions to obesity. Knowledge about these mechanisms can be utilized to find novel anti-obesity drug targets. Our research aims to decipher these mechanisms by combining identification of new brain chemicals and new brain regions that regulate feeding and body weight with behavioral studies aimed at understanding behavioral processes that are co-regulated with appetite. The integration of all these aspects allows for a more holistic understanding of body weight regulation and provides opportunities for identification of new treatment targets.
Impact of gut-brain signals on food reinforcement
Reward-driven eating, eating for pleasure and not out of metabolic need, is crucial in the development of overeating and obesity. Neural substrates underlying reward control may differ from those responsible for homeostatic feeding. Reward or motivated behavior is closely linked to the mesocorticolimbic neurocircuitry, especially the ventral tegmental area and its dopaminergic projections to the nucleus accumbens. Increased dopamine release in the accumbens is typically associated with an increase in motivated behavior, and palatable food is known to induce dopamine release in this brain area. Dysfunction of this circuitry can lead to addictive behaviors.
GLP-1 is a key satiety hormone produced in the intestine and in the brainstem in response to food. GLP-1 analogues are now used in the clinic to regulate blood glucose in Type 2 Diabetes patients. Despite the widespread clinical use of GLP-1 analogues, combined with the fact that they cross the blood brain barrier to reach the brain, surprisingly little is known about the impact of GLP-1 on the brain. We discovered that GLP-1 reduces the reinforcing value of food and does so by stimulating GLP-1 receptors directly on neurons in the mesolimbic circuitry (Journal of Neuroscience 2012). This finding challenged the view that GLP-1 is simply a glucoregulatory and homeostatic hormone, and opened up new therapeutic applications for the GLP-1 analogues. This novel action of GLP-1 analogues is now pursued in clinical trials.
Identifying new neurochemical signals regulating feeding behavior and body weight
Another line of research in my laboratory focuses on finding new brain neurochemicals that are engaged by satiety hormones. We found an unexpected link between GLP-1 and brain cytokines (PNAS 2013): the clinically utilized GLP-1 analogue, Exendin-4, employs two immune system associated molecules – interleukins 1 and 6, in brain areas key for food intake regulation. We showed that this interaction is crucial for the beneficial food intake reducing effect of GLP-1. These findings paved the way to reconsidering brain immune signaling as a part of normal physiological component in regulation of body weight. We are now following up on this work to find whether other peripheral signals may use brain interleukins to reduce food intake, placing interleukins 1 and 6 as integral regulators of body weight.
Brain serotonin signaling is well known to reduce appetite. Overwhelming majority of obesity research focuses on the 5HT2C receptor, it is also the receptor believed to be key to the anti-obesity effect of the pharmaceutical – lorcaserin. Our recent findings (Diabetes 2017), however, suggest that it is the 5HT2A, and not 5HT2C receptor, in the CNS that is being activated downstream of GLP-1 receptor stimulation, to reduce food intake and body fat. This result is unexpected, and certainly warrants future research focusing on the 5HT2A receptor and ways its activity can be harnessed to reduce body weight, an idea we are currently actively pursuing.
The sex gap in preclinical obesity research and its consequences
Nearly half of the obese patient population is female, yet virtually all preclinical research on how the brain’s neural circuitry controls appetite and leads to obesity is done exclusively in male animals. That means that much of what we know about the mechanisms that steer overeating may not be entirely relevant to half of the human population. This is a problem since males and females, humans and rodents alike, may detect and respond to signals controlling eating differently. Understanding these differences may be crucial to finding new effective anti-obesity treatments and ignoring them likely already led to discarding treatments that may have been effective in women but were without much effect in men. In this project we aim to understand how the female gut communicates with the brain to control appetite and body weight and lastly how and why this communication fails in obesity. We also want to know to what degree this communication differs between females and males. In line with the idea of sex differences in CNS control of metabolism, our new rodent studies suggest that behavioral and metabolic responses of females to GLP-1 and testosterone differ from the well-established responses in males (PNAS 2015, Neuropharmacology 2016, Biology of Sex Differences 2016).
Food, and neurochemicals engaged by food, affect far more than just feeding behavior
There is a strong positive correlation between food reinforcement behavior and impulsivity, but the mechanisms behind this relationship remain unknown. Our recent work provides the first demonstration that the stomach-produced hormone, ghrelin, increases impulsivity and also indicates that ghrelin can change two major components of impulsivity – motor and choice impulsivity (Neuropsychopharmacology 2016). This is the first study to link an endogenous appetite-promoting gut-brain signal, ghrelin, to impulsive behavior in rodents.
In another study, we found that chronic treatment with GLP-1 reduces depression-like behavior in rodents and affects serotonergic signaling in brain areas normally associated with emotionality control (Psychoneuroendocrinology 2016). These preclinical results may have direct relevance to patients, if confirmed in a clinical study, and indicate that GLP-1 analogues may be especially useful for obese patients manifesting with comorbid depression.
Key Publications
PubMed: Karolina Skibicka
2020
López-Ferreras L, Eerola K, Shevchouk OT, Richard JE, Nilsson FH, Jansson LE, Hayes MR, Skibicka KP. (2020) “The supramammillary nucleus controls anxiety-like behavior; key role of GLP-1R” Psychoneuroendocrinology.
Bake T, Le May MV, Edvardsson CE, Vogel H, Bergström U, Albers MN, Skibicka KP, Farkas I, Liposits Z, Dickson SL. (2020) “Ghrelin Receptor Stimulation of the Lateral Parabrachial Nucleus in Rats Increases Food Intake but not Food Motivation.” Obesity.
2019
Mishra D, Richard JE, Maric I, Porteiro B, Häring M, Kooijman S, Musovic S, Eerola K, López-Ferreras L, Peris E, Grycel K, Shevchouk OT, Micallef P, Olofsson CS, Wernstedt Asterholm I, Grill HJ, Nogueiras R, Skibicka KP. (2019) “Parabrachial Interleukin-6 Reduces Body Weight and Food Intake and Increases Thermogenesis to Regulate Energy Metabolism.” Cell Reports.
Wang Y, Fathali H, Mishra D, Olsson T, Keighron JD, Skibicka KP, Cans AS. (2019) “Counting the Number of Glutamate Molecules in Single Synaptic Vesicles.” J Am Chem Soc.
Wang Y, Mishra D, Bergman J, Keighron JD, Skibicka KP, Cans AS. (2019). “Ultrafast Glutamate Biosensor Recordings in Brain Slices Reveal Complex Single Exocytosis Transients.” ACS Chem Neurosci.
Anesten F, Dalmau Gasull A, Richard JE, Farkas I, Mishra D, Taing L, Zhang F, Poutanen M, Palsdottir V, Liposits Z, Skibicka KP, Jansson JO. (2019) ”Interleukin-6 in the central amygdala is bioactive and co-localised with glucagon-like peptide-1 receptor.” J Neuroendocrinol.
Anesten F, Mishra D, Dalmau Gasull A, Engström-Ruud L, Bellman J, Palsdottir V, Zhang F, Trapp S, Skibicka KP, Poutanen M, Jansson JO. (2019). ” Glucagon-Like Peptide-1-, but not Growth and Differentiation Factor 15-, Receptor Activation Increases the Number of Interleukin-6-Expressing Cells in the External Lateral Parabrachial Nucleus.” Neuroendocrinology.
López-Ferreras L, Eerola K, Mishra D, Shevchouk OT, Richard JE, Nilsson FH, Hayes MR, Skibicka KP. (2019) “GLP-1 modulates the supramammillary nucleus-lateral hypothalamic neurocircuit to control ingestive and motivated behavior in a sex divergent manner.“ Molecular Metabolism.
2018
López-Ferreras L, Richard JE, Noble E, Eerola K, Anderberg RH, Nilsson FH, Olandersson K, Kanoski SE, Hayes MR, Skibicka KP. (2018) “Lateral hypothalamic GLP-1 receptors are critical for the control of food reinforcement, ingestive behavior and body weight” Molecular Psychiatry.
Langhans W, Adan R, Arnold M, Banks WA, Card JP, Dailey MJ, Daniels D, de Kloet AD, de Lartigue G, Dickson S, Fedele S, Grill HJ, Jansson JO, Kaufman S, Kolar G, Krause E, Lee SJ, Le Foll C, Levin BE, Lutz TA, Mansouri A, Moran TH, Pacheco-López G, Ramachandran D, Raybould H, Rinaman L, Samson WK, Sanchez-Watts G, Seeley RJ, Skibicka KP, Small D, Spector AC, Tamashiro KL, Templeton B, Trapp S, Tso P, Watts AG, Weissfeld N, Williams D, Wolfrum C, Yosten G, Woods SC. (2018) ”New horizons for future research - Critical issues to consider for maximizing research excellence and impact.” Mol Metab.
2017
Anderberg RH, Richard JE, Eerola K, Ferreras LL, Nordbeck EB, Hansson C, Nissbrandt H, Berqquist F, Gribble FM, Reimann F, Wernstedt-Asterholm I, Lamy C, Skibicka KP. (2017). ”Glucagon-Like Peptide-1 and its Analogues Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight” Diabetes, in press
López-Ferreras L, Richard JE, Anderberg RH, Nilsson FH, Olandersson K, Kanoski SE, Skibicka KP. (2017) “Ghrelin’s control of food reward and body weight in the lateral hypothalamic area is sexually dimorphic” Physiology and Behavior, in press
Richard JE, López-Ferreras L, Anderberg RH, Olandersson K, Skibicka KP. (2017) Estradiol is a critical regulator of food-reward behavior Psychoneuroendocrinology, in press
Johannessen H, Revesz D, Kodama Y, Cassie N, Skibicka KP, Barrett P, Dickson S, Holst J, Rehfeld J, van der Plasse G, Adan R, Kulseng B, Ben-Menachem E, Zhao CM, Chen D.Vagal Blocking for Obesity Control: a Possible Mechanism-Of-Action. Obesity Surgery 2017 Jan;27(1):177-185.
2016
Anderberg RH, Hansson C, Fenander M, Richard JE, Dickson SL, Nissbrandt H, Bergquist F, Skibicka KP. The Stomach-Derived Hormone Ghrelin Increases Impulsive Behavior. Neuropsychopharmacology. 2016 Apr. 41(5):1199-209.
Vogel H, Wolf S, Rabasa C, Rodriguez-Pacheco F, Babaei CS, Stöber F, Goldschmidt J, DiMarchi RD, Finan B, Tschöp MH, Dickson SL, Schürmann A, Skibicka KP. GLP-1 and estrogen conjugate acts in the supramammillary nucleus to reduce food-reward and body weight. Neuropharmacology. 2016 Nov;110(Pt A):396-406.
Kanoski SE, Hayes MR, Skibicka KP. GLP-1 and weight loss: unraveling the diverse neural circuitry. American Journal of Physiology Regul Integr Comp Physiol. 2016 May 15;310(10):R885-95.
Richard JE, Anderberg RH, López-Ferreras L, Olandersson K, Skibicka KP. Sex and estrogens alter the action of glucagon-like peptide-1 on reward. Biol Sex Differ. 2016 Jan 16;7:6.
Anderberg RH, Richard JE, Hansson C, Nissbrandt H, Bergquist F, Skibicka KP. GLP-1 is both anxiogenic and antidepressant; divergent effects of acute and chronic GLP-1 on emotionality. 2016 Mar;65:54-66.
Anesten F, Holt MK, Schéle E, Pálsdóttir V, Reimann F, Gribble FM, Safari C, Skibicka KP, Trapp S, Jansson JO. Preproglucagon neurons in the hindbrain have IL-6 receptor-α and show Ca2+ influx in response to IL-6. Am J Physiol Regul Integr Comp Physiol. 2016 Jul 1;311(1):R115-23.
2015
Hu M, Richard JE, Maliqueo M, Kokosar M, Fornes R, Benrick A, Jansson T, Ohlsson C, Wu X, Skibicka KP*, Stener-Victorin E*. Maternal testosterone exposure increases anxiety-like behavior and impacts the limbic system in the offspring. PNAS USA. 2015 Nov 17;112(46):14348-53.
Richard JE, Anderberg RH, Göteson A, Gribble FM, Reimann F, Skibicka KP. Activation of the GLP-1 receptors in the nucleus of the solitary tract reduces food reward behavior and targets the mesolimbic system. PLoS One. 2015 Mar 20;10(3):e0119034.
2014
Richard JE, Farkas I, Anesten F, Anderberg RH, Dickson SL, Gribble FM, Reimann F, Jansson JO, Liposits Z, Skibicka KP GLP-1 receptor stimulation of the lateral parabrachial nucleus reduces food intake: neuroanatomical, electrophysiological and behavioral evidence. 2014 Nov;155(11):4356-67.
Anderberg RH, Anefors C, Bergquist F, Nissbrandt H, Skibicka KP. Dopamine signaling in the amygdala, increased by food ingestion and GLP-1, regulates feeding behavior. Physiology and Behavior. 2014 Sep;136:135-44.
Hansson C, Alvarez-Crespo M, Taube M, Skibicka KP, Schmidt L et al. (2014) Influence of ghrelin on the central serotonergic signaling system in mice. Neuropharmacology 79:498-505.
2013
Shirazi R, Palsdottir V, Collander J, Anesten F, Vogel H, Langlet F, Jaschke A, Schurmann A, Prevot V, Shao R, Jansson J, Skibicka KP. (2013) Glucagon-like peptide 1 receptor induced suppression of food intake, and body weight is mediated by central IL-1 and IL-6. PNAS USA 110: 16199-16204.
Shirazi RH, Dickson SL, Skibicka KP (2013) Gut peptide GLP-1 and its analogue, Exendin-4, decrease alcohol intake and reward. PLoS One 8: e61965.
Skibicka KP (2013) The central GLP-1: implications for food and drug reward. Front Neurosci 7: 181. Review article.
Romero-Pico A, Vazquez MJ, Gonzalez-Touceda D, Folgueira C, Skibicka KP, et al. (2013) Hypothalamic kappa-opioid receptor modulates the orexigenic effect of ghrelin. Neuropsychopharmacology 38: 1296-1307.
Skibicka KP, Dickson SL (2013) Enteroendocrine hormones-central effects on behavior. Curr Opin Pharmacol 13: 977-982. Review article.
Skibicka KP, Shirazi RH, Rabasa-Papio C, Alvarez-Crespo M, Neuber C, et al. (2013) Divergent circuitry underlying food reward and intake effects of ghrelin: dopaminergic VTA-accumbens projection mediates ghrelin's effect on food reward but not food intake. Neuropharmacology 73: 274-283.
Menzies JR, Skibicka KP, Leng G, Dickson SL (2013) Ghrelin, reward and motivation. Endocr Dev 25: 101-111. Review article.
2012
Hansson C, Shirazi RH, Naslund J, Vogel H, Neuber C, Holm G, Anckarsater H, Dickson, SL, Eriksson E, Skibicka KP (2012) Ghrelin influences novelty seeking behavior in rodents and men. PLoS One 7: e50409.
Dickson SL, Shirazi RH, Hansson C, Bergquist F, Nissbrandt H, Skibicka KP (2012) The glucagon-like peptide 1 (GLP-1) analogue, exendin-4, decreases the rewarding value of food: a new role for mesolimbic GLP-1 receptors. J Neurosci 32: 4812-4820.
Alvarez-Crespo M, Skibicka KP, Farkas I, Molnar CS, Egecioglu E, et al. (2012) The amygdala as a neurobiological target for ghrelin in rats: neuroanatomical, electrophysiological and behavioral evidence. PLoS One 7: e46321.
Menzies JR, Skibicka KP, Dickson SL, Leng G (2012) Neural Substrates Underlying Interactions between Appetite Stress and Reward. Obes Facts 5: 208-220.
Cardona Cano S, Merkestein M, Skibicka KP, Dickson SL, Adan RA (2012) Role of ghrelin in the pathophysiology of eating disorders: implications for pharmacotherapy. CNS Drugs 26: 281-296.
Menzies JR, Skibicka KP, Egecioglu E, Leng G, Dickson SL (2012) Peripheral signals modifying food reward. Handb Exp Pharmacol: 131-158.
Skibicka KP, Shirazi RH, Hansson C, Dickson SL (2012) Ghrelin interacts with neuropeptide Y Y1 and opioid receptors to increase food reward. Endocrinology 153: 1194-1205.
Skibicka KP, Hansson C, Egecioglu E, Dickson SL (2012) Role of ghrelin in food reward: impact of ghrelin on sucrose self-administration and mesolimbic dopamine and acetylcholine receptor gene expression. Addict Biol 17: 95-107.
2011
Skibicka KP, Alhadeff AL, Leichner TM, Grill HJ (2011) Neural controls of prostaglandin 2 pyrogenic, tachycardic, and anorexic actions are anatomically distributed. Endocrinology 152: 2400-2408.
De Jonghe BC, Hayes MR, Banno R, Skibicka KP, Zimmer DJ, et al. (2011) Deficiency of PTP1B in POMC neurons leads to alterations in energy balance and homeostatic response to cold exposure. Am J Physiol Endocrinol Metab 300: E1002-1011.
Skibicka KP, Hansson C, Alvarez-Crespo M, Friberg PA, Dickson SL (2011) Ghrelin directly targets the ventral tegmental area to increase food motivation. Neuroscience 180: 129-137.
Skibicka KP, Dickson SL (2011) Ghrelin and food reward: the story of potential underlying substrates. Peptides 32: 2265-2273.
Dickson SL, Egecioglu E, Landgren S, Skibicka KP, Engel JA, et al. (2011) The role of the central ghrelin system in reward from food and chemical drugs. Mol Cell Endocrinol 340: 80-87.
Egecioglu E, Skibicka KP, Hansson C, Alvarez-Crespo M, Friberg PA, et al. (2011) Hedonic and incentive signals for body weight control. Rev Endocr Metab Disord 12: 141-151.
2010
Dickson SL, Hrabovszky E, Hansson C, Jerlhag E, Alvarez-Crespo M, Skibicka KP et al. (2010) Blockade of central nicotine acetylcholine receptor signaling attenuate ghrelin-induced food intake in rodents. Neuroscience 171: 1180-1186.
Egecioglu E, Jerlhag E, Salome N, Skibicka KP, Haage D, et al. (2010) Ghrelin increases intake of rewarding food in rodents. Addict Biol 15: 304-311.
Hayes MR, Skibicka KP, Leichner TM, Guarnieri DJ, DiLeone RJ, et al. (2010) Endogenous leptin signaling in the caudal nucleus tractus solitarius and area postrema is required for energy balance regulation. Cell Metab 11: 77-83.
Zheng H, Patterson LM, Rhodes CJ, Louis GW, Skibicka KP, et al. (2010) A potential role for hypothalamomedullary POMC projections in leptin-induced suppression of food intake. Am J Physiol Regul Integr Comp Physiol 298: R720-728.
2009
Skibicka KP, Grill HJ (2009) Hypothalamic and hindbrain melanocortin receptors contribute to the feeding, thermogenic, and cardiovascular action of melanocortins. Endocrinology 150: 5351-5361.
Skibicka KP, Alhadeff AL, Grill HJ (2009) Hindbrain cocaine- and amphetamine-regulated transcript induces hypothermia mediated by GLP-1 receptors. J Neurosci 29: 6973-6981.
Hayes MR, Skibicka KP, Bence KK, Grill HJ (2009) Dorsal hindbrain 5'-adenosine monophosphate-activated protein kinase as an intracellular mediator of energy balance. Endocrinology 150: 2175-2182.
Skibicka KP, Grill HJ (2009) Hindbrain leptin stimulation induces anorexia and hyperthermia mediated by hindbrain melanocortin receptors. Endocrinology 150: 1705-1711.
2008
Hayes MR, Skibicka KP, Grill HJ (2008) Caudal brainstem processing is sufficient for behavioral, sympathetic, and parasympathetic responses driven by peripheral and hindbrain glucagon-like-peptide-1 receptor stimulation. Endocrinology 149: 4059-4068.
Skibicka KP, Grill HJ (2008) Energetic responses are triggered by caudal brainstem melanocortin receptor stimulation and mediated by local sympathetic effector circuits. Endocrinology 149: 3605-3616.
2007
Grill HJ, Skibicka KP, Hayes MR (2007) Imaging obesity: fMRI, food reward, and feeding. Cell Metab 6: 423-425.
Grants and Awards
Active research grants as Principal Investigator
- Swedish Research Council (2015-2019)
- Rangar Söderberg Foundation (2015-2019) - Fellow in Medicine
- Novo Nordisk Foundation - Excellence Award (2013-2018)
Past research grants as Principal Investigator
- Sahlgrenska Academy Faculty Grant (2011 – 2015)
- Harald och Greta Jeanssons Foundation (2014)
- Swedish Research Council (2012-2014). Ref 20113056
- Harald och Greta Jeanssons Foundation (2013)
- Post-doctoral fellowship, Swedish Institute (2009-2011)
- Pre-doctoral fellow, individual NRSA award, NIH/NINDS: F31-NS059254-01 (2007-2010)
- American Society for Microbiology Undergraduate Research Fellow (2002-2003)
Awards
- The Fernström Prize in Medicine – young investigator 2016
- NIDA - Frontiers in Addiction Travel Award 2012
- Society for the Study of Ingestive Behavior - Travel Award 2011
- Endocrine Society - Award for an Outstanding Publication 2010
News and media
Why you should NEVER make a decision when you're hungry: Hormones make you impulsive and unable to resist temptation
Daily Mail [May 11, 2016]
Hormones that are released during hunger affect decision making
Science Daily [May 9, 2016]
Don't make important decisions on empty stomach
The Times of india [May 10, 2016]
Hormon som utsöndras vid hunger påverkar beslutsförmågan och impulskontrollen
Dagens Diabetes [5 maj 2016]
5 million DKK to take next step toward new treatment for obesity and appetite
Akademiliv [April 17, 2013]
Drugs Made From Gila Monster Lizard Saliva ‘Reduces Food Cravings'
Huffington Post [May 16, 2012]
Drugs from gila monster lizard saliva reduces cravings for chocolate and ordinary food
Science Daily [May 15, 2012]
Ödlesaliv kan hjälpa mot matsug
Dagens nyheter [20 april, 2012]
Ödlesaliv kan dämpa alkoholsug
Göteborgs-Posten [20 april, 2012]
Stomach hormone can fuel or suppress rats’ sugar cravings: Chemical associated with appetite also activates the brain’s pleasure center
Science Daily [November 15, 2010]
