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Metabolism and Energy Balance, Slides of Anatomy

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.

Typology: Slides

2020/2021

Available from 08/18/2024

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Dr. John Redden
Physiology and Neurobiology
University of Connecticut
UNIT9: METABOLISM
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Download Metabolism and Energy Balance and more Slides Anatomy in PDF only on Docsity!

Dr. John Redden Physiology and Neurobiology University of Connecticut

UNIT9: METABOLISM

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:

  • Arcuate Nucleus
  • Paraventricular Nucleus

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

X

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)

Glycogen Synthase

Modifies a glucose-derived molecule so that it can be incorporated into Glycogen.

Glycogen Phosphorylase

Phosphorylates Glycogen Forming Glucose-1-Phosphate (Becomes G-6-Phosphate)

Glucose-6-Phosphatase

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

  • Synthesized in Digestive System

VLDL

  • Made in Liver

LDL

  • Delivers Cholesterol to Tissues
  • Formed from VLDL in Blood

HDL

  • Made in Liver & Small Intestine
  • Accepts Cholesterol

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