Julio Ayala, PhD and Matthew Robinson, PhD discuss their research focusing on high-fat feeding behavior in mice and the effects of stress and exercise on metabolism and obesity.
Obesity and the Metabolic Response to Stress
Julio Ayala, PhD
Stress is a ubiquitous environmental factor that can affect a variety of behaviors, such as feeding. While some individuals reduce their caloric intake in response to stress, most people increase their caloric intake in response to stress, particularly intake of foods and beverages high in fat and sugar (i.e. “comfort feeding”). This behavior can be modeled in rodents since rats and mice typically reduce their caloric intake in response to stress unless they are presented with palatable, calorically dense substances. Surprisingly, most preclinical studies assessing the effect of stress on feeding behavior have been conducted in lean rodents. This represents an important clinical knowledge gap since obese individuals are more prone to the negative effects of stress, including increased caloric intake. This research investigates the consequences of obesity on various responses to stress including effects on caloric intake, energy expenditure, substrate oxidation, and locomotor activity. This presentation will explore potential neuronal mechanisms regulating feeding behavior in response to stress and how these mechanisms may be affected in obesity. The focus of this research is the activity of Glucagon-like peptide-1 receptor (Glp1r)-expressing neurons in the lateral septum (LS), a brain region involved in regulating responses to various cues, such as stress. These findings demonstrate specific effects of obesity on stress responses that may be due to changes in the activity of LS Glp1r neurons.
Skeletal Muscle Mitochondrial Protein Adaptations to Obesity and Exercise
Matthew Robinson, PhD
Skeletal muscle mitochondria are the primary site for oxidizing nutrients and generating ATP. Mitochondria adapt through alterations in proteins and respiratory function to changing bioenergetic supply and demand signals. High-dietary fat is a nutrient stimulus for mitochondrial remodeling associated with metabolic disease, including insulin resistance and type 2 diabetes. Exercise training is an energetic demand that drives mitochondrial remodeling alongside improvements in metabolic health. Changes in mitochondrial lipid oxidation are critical considerations in the development and reversal of skeletal muscle health with obesity. Within that context, the electron transfer flavoprotein and complex I are a critical nexus site for lipid oxidation. This webinar will present data from on-going investigations into mitochondrial protein remodeling to nutrient and exercise demands.
Key Topics Include:
- Learn about the effects of stress and obesity on feeding behavior and other components important to changes in body weight.
- Introduce techniques for measuring real-time neuronal activity in freely-behaving mice
- Understand methodological approaches for mitochondrial respiration
- Identify changes in mitochondrial proteins and respiration with high-fat feeding and exercise
- Translate results from pre-clinical mouse studies to human physiology
Who Should Attend?
Anyone with an interest in measuring metabolic activity, feeding behavior, and energy balance in small animals will be particularly interested in this presentation.
Molecular Physiology & Biophysics
Oregon State University