Chapter 4: Cellular Biology - Energetics

Body Mass Index (BMI)

(Weight in lbs × 703) / (Height in inches)²

i.e: 215 lbs, 76 inches → 26.16

appetite control theories

• Glucostatic Theory: Based on blood glucose levels.

• Lipostatic Theory: Based on body fat content; leptin released when fat increases, reducing appetite.

What factors regulate peptide-related appetite control?

• Hormones (e.g., leptin, ghrelin)

• Neural signals

• Sensory inputs (smell, sight)

First Law of Thermodynamics

∆ Energy = Energy Intake – Energy Output

• Energy Intake = Diet

• Energy Output = Work (transport, mechanical, chemical) + Heat

energy content of macronutrients

• Fat = 9 kcal/g

• Protein = 4 kcal/g

• Carbohydrate (CHO) = 4 kcal/g

indirect calorimetry

Measures oxygen consumption and CO₂ production.

RQ values:

• CHO = 1.0

• Protein = 0.8

• Fat = 0.7

factors that influence Basal Metabolic Rate (BMR)

• Age and Sex

• Lean Body Mass

• Hormones

• Genetics

• Activity Level

• Thermic Effect of Eating

Fed State (Absorptive)

Energy is absorbed, used, and stored (Anabolism).

Fasted State

Stored energy is used (Catabolism).

glycogenesis

glucose stored as glycogen

α-cells

secrete Glucagon

β-cells

produce insulin

δ-cells

Somatostatin

Glucagon

Increases glycogenolysis, gluconeogenesis (liver).

Insulin

• Promotes glucose, amino acid, and fatty acid uptake into cells for storage

Somatostatin

Inhibits insulin, glucagon release; slows GI motility.

Epinephrine

Promotes glycogenolysis and lipolysis.

Cortisol

Antagonizes insulin action.

GLP-1

Enhances insulin secretion, delays gastric emptying, reduces appetite.

Leptin

• Signals energy adequacy to CNS, reduces appetite.

glycogen phosphorylase signaling cascade

• Triggered by cAMP via glucagon/epinephrine → activates glycogen breakdown.

glucose control in fed states

High insulin, low glucagon → promotes storage (glycogenesis, lipogenesis).

glucose control in fasted states

• Low insulin, high glucagon → promotes energy mobilization (glycogenolysis, gluconeogenesis).promotes energy release and mobilization

pathophysiology of Type I diabetes

Autoimmune destruction of β-cells → no insulin.

pathophysiology of Type II diabetes

Insulin resistance → β-cells initially compensate but fail over time.

protein metabolism in diabetes

Low insulin leads to ↑ amino acids, ↑ free fatty acids (ketosis), ↓ protein synthesis, ↑ glycogenolysis, and ↑ blood glucose.

effects of insulin on protein metabolism

• Transports amino acids into cells.

• Promotes protein synthesis.

  • Maintains positive nitrogen balance.

heat balance and thermoregulation

• Homeostasis of temperature maintained via reflexes.

• Mechanisms: Sweating, vasodilation, vasoconstriction, shivering.

glycogenolysis

glucose in metabolism is broken down to glucose

gluconeogenesis

glucose is synthesized from non-CHO

glycolysis

glucose is used metabolically