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A comprehensive overview of the fundamental concepts of metabolism and energy balance. It covers the key mechanisms and regulatory processes involved in the storage, utilization, and conversion of different macronutrients (carbohydrates, fats, and proteins) to meet the body's energy needs. The document delves into the short-term and long-term regulation of appetite and satiety, the role of hormones like leptin and insulin in energy homeostasis, and the implications of metabolic dysregulation in conditions like diabetes. It also explores the complex interplay of genetic, environmental, and behavioral factors contributing to the growing prevalence of obesity. This resource offers valuable insights into the intricate physiological and neurobiological underpinnings of energy metabolism, making it a valuable reference for students and researchers in the fields of physiology, nutrition, and metabolic health.
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Dr. John Redden Physiology and Neurobiology University of Connecticut
ENERGY BALANCE
Energy (^) in
Fat Stores
Energy (^) out “Life Sustaining Chemical Transformations”
Carbs Fats Proteins
Absorption
Metabolic Rate (30-60%) Physical Activity (10-60%) Thermoregulation (10%)
Oxidation/Reduction
REGULATION OF INTAKE
Satiety No Desire For Food
Hunger Desire For Food
Orchestrated By Gut-Brain Axis
SHORT TERM REGULATION: SATIETY
Appetite Suppressants:
1. Vagus Stimulation (Afferent) - Distension of Gut 2. Anorexic Hormones/Peptides - GI Organs - Insulin - CCK - VIP - Adipose Tissue - Leptin Target:
Hypothalamus:
SHORT TERM REGULATION
LONG TERM REGULATION
Energy In = Energy Out…..?
The Lipostatic Theory:
Signals from FAT (adipose) tissue modulate eating behavior in order to maintain a particular weight
LEPTIN: “THE OBESITY GENE” (?)
THE GLUCOSTATIC THEORY
“Fed State vs. Fasted State”
Fed (Absorptive) State:
High Plasma Glucose
Increased Synthesis
Fasted (Post Absorptive) State:
Low
Increased Catabolism
GLUCOSE IS FUEL FOR THE BODY
(Glucose)
Modifies a glucose-derived molecule so that it can be incorporated into Glycogen.
Phosphorylates Glycogen Forming Glucose-1-Phosphate (Becomes G-6-Phosphate)
Dephosphorylates G-6-P, Forming Glucose
GLUCOSE YIELDS (A LOT) OF ATP
HOW DO WE USE FATS?
Fatty Acids (From Triglyceride Stores or Chylomicrons)
CAN be used for energy production ( via Beta Oxidation )
CAN be stored in ADIPOSE tissues (Lipoprotein Lipase)
CAN be released from Adipose Tissues (Hormone Sensitive Lipase)!
LIPOPROTEIN METABOLISM
Chylomicrons & Associated Lipoproteins
Chylomicrons
VLDL
LDL
HDL
Apolipoprotein
ApoB/C (^) ApoB/C ApoA
FASTING METABOLISM
Begins Overnight or Several Hours of Fasting
Goal: Stay Glucostatic
Approximately 5% of the Liver Weight , and 2% of Skeletal Muscle Weight is Glycogen
Liver glycogen stores
Free fatty acids
Ketone Glucose bodies
Energy production
Glycogenolysis^ b -oxidation
GLYCOGEN CONVERTS TO GLUCOSE
Only hepatocytes express glucose-6-phosphatase
The Liver and Skeletal Muscle Contain Glycogen Phosphorylase
Glucose Levels in The Blood Increase