Physiology of Energy Management

Welcome to the Pediatric Obesity Column for JPSN! This column’s mission is to provide information and resources to the pediatric surgical nurse caring for children affected by obesity and to share focused assessment and intervention strategies that can be incorporated into the practitioner’s daily practice. Research and knowledge about the body’s energy regulatory systems and consequences of damage to these systems are evolving rapidly. Although in the early stages, it is clear that an understanding of our bodies’ many energy regulatory systems, including how they are damaged and by what, will lead to better management and treatment of obesity. In this column, we will review the physiology of normal energy metabolism and then touch on three pertinent neurohormonal pathways that contribute to energy balance. In the next column, we will examine some of the pathophysiology that occurs when these energy systems function incorrectly. As an in-depth discussion in this column’s format is not appropriate, we will touch only broadly on energy regulation and pathophysiology. The reader is encouraged to utilize the reference list, bibliography, and Webinar recommendations for further information. Energy management is essential to life and continuation of our species. As a result, we have several redundant systems to ensure that there is always a backup system. Many of these systems have been studied and taught for years (remember Kreb’s cycle?). The obesity epidemic, when seen as an energy system gone awry, forces us to reexamine long-held beliefs and consider a different paradigm. When food is ingested, the body needs to convert it to a form that cells can use for energy. In addition, our energy systems are designed to store energy in the event of a long-term (famine) or short-term (the chasing bear) need. The body also adapts to normal biological states such as adolescence/puberty and pregnancy that require increased energy for new growth and development. On the macro level, food is ingested and broken down by a series of enzymes to its most basic components: sucrose, amino acids, and free fatty acids. We will mainly focus on sucrose and how increased circulating amounts may affect our energy systems. Sucrose is broken down during digestion to glucose and fructose. In normal circumstances, glucose is processed in the small intestine and then transported to the liver for continued processing and distribution. The liver uses some glucose for itself, some is converted to glycogen for “a rainy day,” and the rest is sent via the circulatory system for use by other organs. Fructose, however, goes directly to the liver for processing. In small amounts at reasonable intervals, the liver is able to handle both glucose and fructose metabolism. However, when increased and steady amounts of glucose and fructose are presented to the liver, energy processing systems can become overwhelmed with maladaptive energy storage and organ damage the result (Lustig, 2012). Fiber, when ingested in appropriate amounts, increases transit time of nutrients being broken down in the small intestine. Benefits of increased transit time include less nutrient exposure to small bowel surface area with less resulting nutrient absorption. Nutrients reach the distal small bowel faster and stimulate increased peptide YY and glucagon-like peptide-1 production, signaling to the hypothalamus that you are full and to stop ingesting more energy/food (Lustig, 2012). The hypothalamus controls the master plan and identifies, interprets, and directs energy intake, metabolism, and storage through feedback from several systems. The three neurohormonal systems discussed here are hunger, hedonic, and stress (Lustig, 2012). HUNGER The primary function of the ventromedial hypothalamus, a subarea of the hypothalamus, is to manage energy storage and expenditure. Feedback is received from the gastrointestinal tract and adipose cells by the neurohormones leptin and insulin. If energy stores are perceived as adequate, the anorexigenesis signal is given. This turns on the sympathetic nervous system (SNS), increasing muscle activity and fat loss. It also turns off the parasympathetic nervous system (vagus nerve), decreasing appetite and fat storage. When the ventromedial hypothalamus perceives inadequate energy stores, the opposite reaction, orexigenesis, occurs. Insulin plays a primary role in these processes by unlocking cells that allow the energy source to enter and subsequently be utilized or stored. HEDONIC The hedonic pathway is a neural connection between two brain areas, the ventral tegmental area and the nucleus accumbens (NA or reward center). These structures are responsible for species’ survival, rewarding food intake for nourishment and sex for reproduction, both basic needs of the species. The reward occurs when the ventral tegmental area signals the NA to release dopamine after energy ingestion. The dopamine that is released binds to a D2 receptor in the NA, and a sense of pleasure results. Dopamine expression is then suppressed by leptin, which signals that energy needs are met, causing the sense of pleasure to fade. STRESS The stress response is essential to life, keeping us vigilant and responsive to our environment. It is coordinated in the area of the brain known as the amygdala. The amygdala responds to input through activation (or deactivation) of two primary systems: cortisol released by the adrenal gland and/or activation of the SNS. When activated, both cortisol and the SNS elevate blood glucose, increase blood pressure, and prepare the body to meet the perceived stressor. After the stressor is eliminated, the systems return to their normal state. This system is designed for acute situations with short bursts of exposure to cortisol and SNS activation. The broadness of the normal physiology descriptions of these three energy systems reflects the scope of this column. The reader is encouraged to explore this physiology further as a foundation for next quarter’s column, where the mechanisms by which and consequences (metabolic syndrome and obesity) of these pathways going awry will be examined. Further reading and Webinars offering more depth and background to energy management are listed in the bibliography. This is an exciting time for those affected by obesity. Emerging research on why these energy systems are breaking down, who is susceptible, whether they are reversible, what treatment(s) will effectively treat which symptoms, and how to support patients through this experience is challenging us to rethink and reframe our traditional perceptions of obesity (Ochner, Tsai, Kushner, & Wadden, 2015). As nurses, we have an opportunity to be at the forefront of this emerging science and contribute to its dissemination to our colleagues and patients.