Metabolism Quiz - Cellular Functions Overview

Gastrointestinal Physiology - Nutrition and Metabolism

• This presentation covers gastrointestinal physiology, focusing on nutrition and metabolism.
• The presenter is Dr. Zülal Kaptan.

Learning Outcomes

• Identify signals from the stomach, brain, and peripheral tissues that regulate hunger and satiety.
• Explain the short-term and long-term mechanisms that regulate food intake.
• Discuss the brain regions involved in feeding behavior.
• Correlate smooth muscle electrophysiology with gastrointestinal (GI) movements.
• Understand the basic concepts of metabolism.
• Differentiate between catabolism and anabolism.
• Understand the use of nutrients in absorptive and postabsorptive periods.
• Understand the relationship between the endocrine system and metabolism.
• Define basal metabolic rate (BMR).
• Identify factors that impact metabolic rate.

Nutritional Requirements

• The body's energy needs must be met by the caloric value of food to prevent the breakdown of its own fat, carbohydrates, and protein.
• Vitamins and minerals are crucial for enzymatic reactions, but do not directly provide energy.

Living Tissue and Energy

• Living tissue requires a continuous energy expenditure.
• Energy is obtained directly from ATP and indirectly from cellular processes, like glucose, fatty acids, ketone bodies, amino acids, and other organic molecules.
• These molecules can also be derived from stored glycogen, fat, and protein within the body.

Food Intake - What Starts a Meal?

• Environmental signals (mealtime, food smells, etc.) can initiate eating.
• Signals from the stomach (ghrelin): Ghrelin levels increase during hunger and decrease after eating. Food entering the duodenum suppresses ghrelin release.
• Metabolic signals (glycoprivation and lipoprivation): Cells lacking glucose and lipids stimulate hunger.

Food Intake - What Stops a Meal?

• Short-term satiety signals occur before food digestion, triggered by stomach, intestine, and liver signaling the brain.
• Long-term satiety signals are associated with fat tissue, which stores nutrients for extended periods.

Brain Mechanisms

• The brain receives hunger and satiety signals.
• The brainstem controls basic chewing and swallowing behaviors.
• The hypothalamus plays a significant role, with the lateral hypothalamus being the hunger center and the ventromedial nucleus being the satiety center.
• The cerebral cortex and amygdala regulate appetite through cognitive factors.

Hypothalamus

• Lateral hypothalamic area: This area is primarily active during hunger states.
• Ventromedial area: This area is active and inhibits the lateral hypothalamus when sufficient nutrients are available.
• The interaction between these areas is crucial.

Hypothalamus - Lesion Effects

• Lesions in the lateral hypothalamus lead to organic anorexia.
• Lesions in the ventromedial nucleus lead to obesity.

Peripheral Signals and Brain Activity

• Sensory information from the gastrointestinal tract initiates satiety feelings.
• Gastrointestinal hormones (e.g., CCK) and blood nutrient levels (e.g., glucose and fatty acids) influence satiety.
• Signals from the cerebral cortex and amygdala also influence feeding behavior.
• Body temperature fluctuations affect appetite, with low temperatures stimulating appetite and higher ones suppressing it.

Metabolic Signals - Glucostatic Hypothesis

• Glucose-sensitive cells (glucostats) in the ventromedial hypothalamus become active with increased blood glucose, inhibiting the lateral hypothalamus.
• This suppression ceases when blood glucose levels decrease.

Metabolic Signals - Lipostatic Hypothesis

• Leptin, released from adipose tissue, affects the brain areas involved in appetite regulation.
• The ventromedial nucleus does not play a vital role in leptin's effects.
• Leptin's effects mostly involve the arcuate, lateral, and paraventricular hypothalamus.

Effects of Leptin Increase

• Elevated leptin directly affects the arcuate nucleus, increasing sympathetic activity in the brainstem.
• This stimulation increases metabolic activity and suppresses appetite.
• It stimulates the paraventricular nucleus, further aiding satiety.
• It triggers the release of appetite-suppressant neuropeptides, such as a-MSH and CART.
• These neuropeptides work to inhibit the lateral hypothalamus.

Digestive Activity Ending

• When digestive activity concludes, leptin levels decrease, initiating appetite stimulation.
• The arcuate nucleus can no longer stimulate the sympathetic system or the paraventricular nucleus.
• The arcuate nucleus releases appetite-stimulating peptides like neuropeptide Y and Agouti-related protein (AgRP).

Additional Peptides and Neurochemicals

• Other peptides are synthesized in the hypothalamus, including MCH (melanocyte-concentrating hormone) and orexin/hypocretin.
• These peptides influence the limbic system and the prefrontal cortex, affecting higher-level cognitive and emotional processes related to food intake.
• Endocannabinoids also increase the release of MCH and orexin.

Summary of Orexigenic and Anorexigenic Molecules

• Orexigenic molecules (NPY, AGRP, MCH, orexin, and endocannabinoids) promote hunger.
• Anorexigenic molecules (a-MSH and CART) combat hunger.

Metabolism

• Metabolism encompasses all chemical reactions within the body.
• It involves two main types: catabolism (breakdown of complex molecules) and anabolism (synthesis of complex molecules).

Catabolism

• Catabolism is an exergonic process (releases energy).
• In catabolism, complex organic molecules are broken down into simpler units.

Anabolism

• Anabolism is an endergonic process (requires energy).
• In anabolism, simple molecules combine to form complex structural and functional components.

Metabolism - Energy Balancing

• Metabolism is characterized by the balanced exchange of energy between catabolic and anabolic reactions.

ATP and Energy Exchange

• ATP plays a pivotal role in energy transfer and exchange within cells.
• Catabolic pathways produce ATP, while anabolic pathways consume ATP.

Catabolism Efficiency

• During catabolism, about 40% of the released energy is utilized for cellular functions, and the remaining energy is released as heat.

Metabolic Adaptations

• Factors impacting metabolic reactions include internal cellular conditions (e.g., oxygen and ATP levels), the nervous and endocrine systems, and the time elapsed since the last meal.

Absorptive State

• During the absorptive state, nutrients are absorbed from the gastrointestinal tract and are used to meet immediate energy demands.
• Key metabolic processes involved include glucose catabolism, catabolism of amino acids and lipids, protein synthesis, glycogen synthesis, and lipogenesis.

Absorptive State Regulation

• GIP and rising blood glucose and amino acid levels stimulate pancreatic beta cells to release insulin.
• Insulin facilitates the movement of glucose and amino acids into cells and promotes glycogen, triglyceride, and protein synthesis.
• Insulin also inhibits catabolic reactions.

Postabsorptive State

• In the postabsorptive state, the energy sources are those stored in the body.
• The primary challenge is maintaining normal blood glucose concentrations.
• Key metabolic mechanisms in this state involve glycogenolysis, lypolysis, gluconeogenesis, and catabolism of fatty acids, amino acids, and ketone bodies.

Homeostasis of Blood Glucose

• Blood glucose levels are crucial for the nervous system. Erythrocytes cannot obtain energy from fatty acids.
• Homeostasis is primarily achieved by the blood glucose concentration, which is critical to the nervous system, retina, and erythrocytes.

Glucose Generation

• The liver is a critical source of glucose during the post-absorptive state through glycogenolysis.
• During the post-absorptive state, skeletal muscles can also experience glycogenolysis, with glucose being utilized for muscle contraction.

Glucose and Energy Production

• Lipolysis occurs in fat tissue, breaking down triglycerides into glycerol and fatty acids that are converted to glucose by the liver.
• Proteins can break down to amino acids, used by the liver for glucose production.
• Different tissues catabolize fuels to provide energy for specific needs.

Glucose Preservation

• During the post-absorptive state, most body cells switch to alternative energy sources other than glucose, preserving more glucose in the blood for organs like the brain and red blood cells.

Fat Metabolism

• Fatty acids released from lipolysis cannot directly produce glucose.
• Cardiac muscle can utilize lactic acid for ATP production.
• Hepatocytes catabolize amino acids to generate ATP.
• Hepatocytes generate ketone bodies from fatty acids, which other tissues can use for ATP production.

Regulation in Post-Absorptive State

• Hormones (e.g., glucagon) and the sympathetic nervous system play crucial roles in regulating post-absorptive metabolism.
• Glucagon is released when blood glucose levels fall, promoting glycogenolysis and gluconeogenesis in the liver.
• The sympathetic nervous system releases norepinephrine and epinephrine, which induce glycogenolysis and lipolysis.

Cortisol Release and Stress

• The adrenal gland releases cortisol in response to stress, which promotes gluconeogenesis, lipolysis, and protein catabolism to maintain blood glucose levels.

Role of Nutrients in Metabolism

• Carbohydrates serve as immediate energy sources that can be stored as glycogen.
• Excess carbohydrates are converted to triglycerides and stored in adipose tissue for long-term energy reserves.
• Protein provides amino acids, which can serve as energy sources (during times of starvation, etc.) or be used to build proteins.
• Lipids (fatty acids and triglycerides) are converted to energy (catabolized) or are part of a long-term storage system.

Basal Metabolic Rate (BMR)

• BMR is an important measure of energy expenditure to maintain basic functions under resting conditions.
• Normal levels are between 1200-1800 kcal/day in adults.

Factors Affecting BMR

• Thyroid hormones (thyroxine and triiodothyronine) are the main regulatory factors.
• Other hormones like testosterone, insulin, and growth hormone also affect BMR, but these effects are often modest.
• Age and sex also influence BMR, with children having higher rates and women outside of pregnancy and lactation having generally lower rates.
• Physical activity, body temperature, and food intake contribute to the overall metabolic rate.

Measuring BMR

• There are two main methods for measuring BMR: direct and indirect calorimetry.