Andrews Lab research
About Professor Zane Andrews
Professor Andrews received his PhD in New Zealand from the University of Otago in 2003 studying the neuroendocrine control of pregnancy and lactation. He undertook postdoctoral training at Yale University, New Haven, Connecticut, USA (2004-2008) with Tamas Horvath. At Yale, he focused on the neural control of appetite and energy metabolism, with a particular emphasis on neurocrine control of ghrelin in the brain. He moved Monash University in Melbourne, Australia in 2009 and established his own laboratory, where he continues to work on neural control of appetite and behaviour and the neuroendocrine actions of ghrelin. He has maintained fellowship funding through the ARC and NHMRC and is currently NHMRC SRF A. He is currently deputy director of the Monash BDI Metabolism, Diabetes and Obesity program.
- Hunger-sensing neural pathways influence appetite and behaviour
- Neural circuitry of food choice: Implications for obesity
- Ghrelin receptor sensing in the brain links hunger to mood and motivation
- Neural sensing of hunger links homeostatic and reward pathways
- Role of PKD in adiposity and the regulation of body
- How does the brain sense low glucose levels and switch on corrective actions?
Visit Professor Andrews' Monash research profile to see a full listing of current projects.
Our lab studies how food, and the lack or food, affects the brain and behaviour. We are primarily interested in understanding the neural circuits that sense hunger or hypoglycemia and influence brain function, including energy homeostasis, glucose homeostasis, mental health and neurodegeneration. It is becoming increasingly clear that a state of hunger elicits numerous effects on the brain, not just those related to food intake. We are interested in how these metabolic neural circuits detect hunger and hypoglycemia and regulate stress and motivation circuits to link states of hunger with mood and motivation. By understanding how these processes work in normal physiological situations, we have the ability to influence the treatment and prevention of obesity, diabetes, eating disorders, anxiety and mood disorders as well as food addiction.
We focus on the hormone ghrelin as a key hormonal signal of hunger and AgRP neurons as key hunger-sensing neurons in the brain and our research over a number of years shows that hunger influences not only metabolism but also many non-food associated behaviours such as anxiety, reward and neuroprotection.
Hunger sensing: Agrp neurons convey energy deficit (hunger) throughout the brain. As well as promoting food intake, Agrp promote adaptative behaviours to enable coping with periods of low food availability. This includes mood, motivation, memory, attention, stress control. We seek to understand how these neurons detect hunger and influence these behaviours.
Agrp neurons represent a common starting point from which the brain spreads a message of hunger Ghrelin is a hormone from the stomach that signals to the brain low food availability. Ghrelin can target multiple brain sites simultaneously.
Hunger-sensing Agrp neurons in the brain are crucial to maintain food intake and a normal body weight. Without these neurons, an organism is at risk of starvation. Hunger-sensing Agrp neurons communicate with numerous different brain regions to help control our response to hunger and energy deficit.
Agrp neurons in the Arcuate nucleus of the hypothalamus
Hunger signaling: Ghrelin is a message (hormone) from the body that tells the brain there is limited food available. Ghrelin is most effective during periods of hunger and least effective in obese individuals. We coined the term ghrelin resistance to describe less. We seek to understand how ghrelin helps the body cope with hunger by influencing physiology and behaviour.
Schematic diagram of the ghrelin axis. Ghrelin is a stomach hormone that informs of the brain and body of low energy availability. in response to sensing low energy availability the brain engages adaptive response to increase hunger and motivation, as well as mechanisms to cope with hunger such as influencing mood, stress, peripheral metabolism and cellular function.
Ghrelin receptors in the dentate gyrus of the hippocampus.
Regulation of food intake, food seeking and behavior: Sensory processing of external cues and emotional state influence appetite. External cues that signal food can drive intake in the absence of hunger whereas changes in emotional state also modulate appetite in the absence of hunger and satiety. We examine the neural circuits responsible.
Adaptive responses to hunger regulated in the brain.
This image illustrates the need to understand how different regions of the brain communicate in order to control appetite. Here we are interested in identifying the circuits controlling emotion, motivation and decision-making interact and how they with metabolic circuits regulating appetite and metabolism.
- Mouse genetics
- Viral genetics
- Neural circuit tracing
- Neural circuit function (Opto and chemogenetics)
- Neural population recording (Fibre Photometry)
- Behavioural Neuroscience including RFID home cage learning and feeding behaviour
- Metabolic Physiology
- Metabolic phenotyping
- Diet-induced obesity
- Type 1 diabetes
We collaborate with many scientists and research organisations around the world. Click on the map to see the details for each of these collaborators (dive into specific publications and outputs by clicking on the dots).
Student research projects
The Andrews Lab offers a variety of Honours, Masters and PhD projects for students interested in joining our group. There are also a number of short term research opportunities available.
Please visit Supervisor Connect to explore the projects currently available in our Lab.