Energy Balance - Rima PDF
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Arabian Gulf University
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This document provides an overview of energy balance, food intake, and body weight. It covers various aspects like energy yielding nutrients, calorimetry, and factors that impact basal metabolic rate (BMR). An understanding of both short-term and long-term regulation of food intake is also included. The document references relevant YouTube videos.
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Regulation of Energy Balance, Food Intake, and Body Weight Year 2 - Unit I Problem 1: Obesity 9/5/2024 Energy Available in Foods - Energy Yielding Nutrients meaning nutrients...
Regulation of Energy Balance, Food Intake, and Body Weight Year 2 - Unit I Problem 1: Obesity 9/5/2024 Energy Available in Foods - Energy Yielding Nutrients meaning nutrients that give energy The stored chemical energy of foods can be released through cellular respiration. - Determining the Energy Content of Food - Calorimetry Combustion of the food source causes the stored energy to be released as heat, which raises the temperature of water. The amount of energy required to raise 1 g of water by 1ºC is 4.2 J or 1 calorie (cal) – this is the specific heat capacity of water. The large calorie, food calorie, or dietary calorie, is the amount of heat required to raise the temperature of 1 kg of water by 1°C. 1 Cal = 1000 cal (1kcal) The heat liberated when food is burned in the air is the same as when food is metabolized in the body. https://www.youtube.com/watch?app=desktop&v=U1_DYV_q9BA https://www.youtube.com/watch?v=PgDxS3cpuX4 Different foods contain different proportions of proteins, CHOs, and fats, therefore supplying different amounts of energy. Energy Available in Foods 9/5/2024 Respiratory Quotient (RQ) During the oxidation of food, the RQ value indicates which macronutrients are being metabolized: RQ = Volume CO2 produced / Volume O2 consumed The respiratory quotient (RQ ) is Carbohydrate same used in calculations the or consumeda therefore it's 100 more same of BMR. consumer protein,oxygena produced more for fat , oxygen consumed is more than produced -withdabetes ,there'saproblemWrization is more than carb You will end up having. RQ less than the normal carbohydrate Most of the time, energy consumption is CHOs = 1 (Completely oxidized) composed of both fats and carbohydrates. Fats = 0.7 (Require more O2 for oxidation) When there is an increase in the rate of Proteins = 0.8 utilization of fat relative to CHOs, the RQ The approximate RQ of a mixed diet is 0.8. decreases (e.g.: Diabetes Mellitus) The minimum amount calorie of energy required by the body to maintain body Factors Affecting BMR functions at complete Basal physical and mental rest in the post-absorptive Height, weight, and surface area Metabolic state (12 - 14 hrs. after Sex Rate the last meal). Age (BMR) Muscular exertion BMR Expression High or low environmental temperature - As Cal/m2/hr. Growth - 2000 kcal/day i.e. (2000 Reproduction Cal/day) Lactation Emotional state Body temperature Disease states ( Increased in infections, leukemia, hypertension,..) Circulating levels of hormones (thyroid & and catecholamines) 9/5/2024 - Specific Dynamic Action (SDA) Phenomenon of the extra heat moreenergprotes gest production by the body, over I & and above the calculated caloric value, when a given food is metabolized by the body Daily Energy Expenditure SDA Associated with digestion and Also known as the absorption of food in thermic effect of food the body. or dietary-induced These processes 8-10% thermic effect of food (SDA) thermogenesis. require energy and 60- 65 % on basal metabolism generate heat. 25% physical activity ' Energy Homeostasis / Balance and Storage Stability of the body’s total mass and composition over periods requires that energy intake matches energy expenditure. Excess energy intake is stored mainly as fat, whereas a deficit of energy intake causes loss of total body mass until energy expenditure eventually equals energy intake. 9/5/2024 Control of Food Intake and Energy Balance The body is endowed with powerful physiological control systems that help maintain adequate energy intake. States of Food Intake Hunger: A sensation that motivates the seeking and consumption of food (eg, rhythmic stomach contraction and restlessness). Satiety: State of being completely satisfied, Neuronal especially with food or pleasure. regulation in the Hormones released from brain mainly in the the gastrointestinal tract Appetite: Desire for food, often a Endocrine or and adipose tissues. Hypothalamus hormonal particular type. hypothalmus : neuronal regulation regulation 9/5/2024 The Hypothalamus and Control of Food Intake Other nuclei in the Hypothalamus Lateral nuclei (Feeding center) 1. Dorsomedial nuclei act as hunger center: destruction or damage of If stimulated: Hyperphagia which depresses eating behavior. Lesion: Emaciation and weight loss (Inanition) 2. Paraventricular nuclei act as satiety center: destruction or damage of which increases eating behavior. Ventro-medial nuclei 3. Arcuate nuclei are the sites for the integration of multiple feeding/energy (Major Satiety center) status-related inputs from the body. Stimulation: Suppresses feeding and aphagia Destruction: Continued eating and extreme obesity 1. Homeostatic Control of Food Intake: Hypothalamic Inputs Neural signals from the GI tract provide sensory information about stomach filling (Through Vagus nerve). Signals released by adipose tissues. Endocrine signals (Gastrointestinal hormones). Metabolic Information: Nutrient levels in the blood (glucose, amino acids, and fatty acids) that signify satiety. 2. Non-Homeostatic (Cognitive and Reward) 9/5/2024 Control of Feeding: Cortex and Limbic areas Multiple behavioral, social, and environmental Regulation of Food Intake factors influence food intake in humans. Short-term Regulation of Food Intake Long-term Regulation of Food Intake For preventing overeating at each meal. For maintenance of normal quantities of energy stores in the body. Rapid feedback signals responsible: 1. Gastrointestinal filling inhibits feeding. Biological feeding control mechanisms linked to the nutritional status of the body: 2. Gastrointestinal Hormonal Factors 1. Glucose, amino acid, and lipid levels affect the CCK: Released in response to fat and proteins entering the neuronal firing rate of feeding and satiety centers duodenum. Contributes to meal cessation. (Glucostatic, aminostatic, and lipostatic theory of Peptide YY (PYY): Secreted by the entire GI tract, especially by hunger/feeding regulation). the ileum and colon. Glucagon–like peptide (GLP) and insulin: Both tend to suppress 2. Temperature regulation and food intake: Low appetite. temperature (cold) increases feeding. Ghrelin: Secreted mainly by the stomach & increases feeding. 3. Feedback signals from adipose tissues regulate food 3. Oral factors or receptors meter food intake. intake. - Leptin Chewing, salivation, swallowing, and tasting “meter” the food as it passes the mouth. Inhibits feeding but of less intensity and of short duration. Hypothalamic Networks for Homeostatic Regulation of Feeding Behavior Neuropeptidergic networks First-order neurons located in the arcuate nucleus, produce either: o Orexigenic neuropeptides (AgRP and NPY) OR o Anorexigenic (appetite diminishing) peptides (POMC and CART)- These neurons project to second-order neurons producing either: o Orexigenic peptides orexin (ORX) and melanin- concentrating hormone (MCH) in the lateral hypothalamus. OR o Anorexigenic factors oxytocin (OT), thyrotropin-releasing hormone (TRH), and corticotropin-releasing hormone (CRH) in the paraventricular nucleus. AgRP/NPY: Agouti-related protein/ Neuropeptide Y POMC/CART: Pro-opiomelanocortin / Cocaine–and amphetamine-regulated transcript Neurotransmitters & Hormones That Influence Hypothalamic Feeding and Satiety Centers α-Melanocyte-stimulating hormone (α-MSH) Leptin Serotonin Decrease Feeding Norepinephrine (Anorexigenic) and Corticotropin-releasing hormone (CRH) Insulin increase energy Cholecystokinin (CCK) (small intestine and CNS) expenditure. Cocaine- and amphetamine-regulated transcript (CART) Peptide YY (PYY) Glucagon-like peptide (GLP) (from small intestine) Neuropeptide Y (NPY) – short lived effects Agouti-related protein (AGRP) Melanin-concentrating hormone (MCH) (from Increase food intake lateral hypothalamus) (Orexigenic) and Orexins A and B Endorphins reduce energy Galanin (GAL) expenditure. Amino acids (glutamate and γ-aminobutyric acid) NPY is the most potent orexigenic peptide Cortisol activated by decreases in leptin. Ghrelin Endocannabinoids Adipose Tissue and Regulation of Food Intake - Role of Leptin The hypothalamus senses energy storage through the action of Leptin, a peptide hormone secreted by white adipose tissue. When fat stores are less, the adipostat signal is low, and the hypothalamus responds by stimulating hunger and decreasing energy expenditure to conserve energy. When fat stores are too much, the signal is increased, and the hypothalamus responds by decreasing hunger and increasing energy expenditure. This takes place by the role played by two genes: the ob gene (obese gene), and its product leptin, and the db gene, (diabetes gene) whose product is the leptin receptor (ObR). Regulation of Energy Balance by Leptin Leptin’s anorexigenic effects mainly by modulating the activity of NPY/AgRP and POMC neurons in the hypothalamic arcuate (ARC) nucleus. 1. Decreasing production of appetite stimulator (NPY, AgRP) by the hypothalamus. 2. Activation of POMC neurons (α-MSH release)- Leptin-Melanocortin Pathway. 3. Increasing corticotropic-releasing hormone (CRH) release (Decreases food intake). 4. Increasing indirectly sympathetic nerve activity. Increased energy 5. Decreasing insulin secretion, leading to less expenditure storage of energy. Insulin is the primary regulator of leptin production/secretion via glucose metabolism. 6. Increasing thermogenesis. 9/5/2024 Obesity Energy intake > Energy expenditure 25% or greater of total body fat in men An excess 35% or greater of total body fat of body fat in women. For each 9.3 calories of excess energy that enters the body, 1 g fat = 9.3 about 1 gram of fat is added. Cal Obesity-associated diseases Subcutaneous tissues Intraperitoneal cavity Cirrhosis Fat is stored Liver and other tissues (in very Hypertension in: obese people) Heart attack Stroke The development of obesity in adults is accompanied by Kidney disease increased numbers, as well as increased size of adipocytes. Diabetes Causes of Obesity 1. Decreased physical activity 2. Abnormal feeding habits (Environmental, social and psychological factors) 3. Childhood over-nutrition: Increase the number of fat cells 3x normal in obese children and also during puberty. 4. Genetic Factors: 20-25% of cases of obesity may be caused by genetic factors causing abnormalities in: One or more of the pathways regulating the feeding center Energy expenditure and fat storage Mutation in melanocortin receptor 4 (MCR4) Leptin (Congenital deficiency) Leptin receptors (Mutations) 5. Neurogenic Abnormalities: Lesions, neurotransmitters, receptors. Mutations that cause obesity in humans are indicated by the solid green arrows. Proprotein convertase 1 (PC-1) Leptin and Obesity Unusually high sustained concentrations of leptin from the enlarged adipose stores result in leptin desensitization. Weight gain in obese people is associated with leptin resistance. Causes of leptin resistance: 1. Changes to leptin receptor signaling, particularly in the arcuate nucleus. 2. Alterations in leptin formation (Dysregulation in leptin expression) 3. Impaired leptin transport across the blood-brain ob/ob mice are characterized by a mutation of the barrier (Saturation of leptin transporters…) obese (ob) gene encoding leptin. db/db mice have a mutation of the diabetes (db) gene encoding for the ObR (leptin receptor). Treatment of Obesity Drugs that directly inhibit feeding centers Drugs for (Amphetamines) decreasing the Stimulation of POMC Decrease energy input degree of neurons to cause satiety < energy expenditure hunger (Bupropion = Dopamine and NE reuptake inhibitor or Synthetic GLP-1 agonists) Reduction in calorie Increase physical intake activity Sodium-glucose transporter 2 (SGLT2) inhibitors: prevent reabsorption of glucose and water in the kidney Surgical treatment for morbidly obese patients Drugs for reducing lipid absorption by the gut: Orlistat ( a lipase inhibitor that reduces intestinal Vertical sleeve digestion of fat) Gastric bypass Gastric banding gastrectomy: removal surgery surgery of a large part of the stomach Inanition, Anorexia, and Cachexia Inanition: The opposite of obesity. Extreme weight loss Anorexia: A reduction in food intake caused caused by inadequate availability of food or by primarily by diminished appetite. pathophysiologic causes. Anorexia nervosa: Abnormal psychic state in which a person loses the desire for food and even becomes nauseated by food. Cachexia: Wasting syndrome. Loss of weight Muscle atrophy Fatigue and weakness Significant loss of appetite in someone who is not actively trying to lose weight (but due to severe chronic illness). Some studies suggest that excessive activation of POMC pathway in the arcuate nuclei and melanocortin receptors-4 (MCR-4) may play a role in causing the loss of appetite for food (anorexia) associated with severe infections, cancer tumors, or uremia. 9/5/2024