Energy Expenditure and Energy Balance

Energy Requirements and Energy Balance

Total Energy Expenditure (TEE)

  • Basal Metabolic Rate (BMR):
      - Definition: Energy needed to sustain basic metabolic functions such as the activity of the brain, heart, gastrointestinal peristalsis, turnover of epithelium, involuntary body motion, protein turnover, and maintenance of osmotic gradients.

  • Thermic Effect of Food (TEF):
      - Definition: The short-term rise in body temperature following a meal. This is associated with the processes of digestion, absorption, transport, and storage of food.

  • Energy Expenditure for Physical Activity (EEPA):
      - Definition: It encompasses all types of physical activity and physical work that contribute to the overall energy expenditure of an individual.

  • Energy Cost of Thermoregulation:
      - Note: Usually not considered significant for humans in the context of total energy expenditure.

Organ Metabolic Activity

  • Metabolic Activity of Organs:
      - Organs exhibit a very high metabolic rate. Significant contributions include:
        - Liver: 27%
        - Brain: 19%
        - Heart: 7%
        - Kidneys: 10%
        - Skeletal Muscle: 18%
        - Other Organs: 19%
      - The sum of the energy expenditures contributes significantly to the Resting Metabolic Rate (RMR).
      - Fat-free Mass Impact:
        - BEE/BMR is largely dependent on the amount of fat-free mass in the body.
      - Trauma or Infection:
        - BEE/BMR increases during hypermetabolic states such as trauma or infection.

Key Determinants of Total Energy Expenditure

  • Genetic Traits: Influence metabolic rate and energy expenditure

  • Physical Activity: Contributes significantly to energy expenditure, ranging from 10-30%

  • Age, Sex, Environmental Stimuli:
        - Age: Affects BMR and potentially TEF
        - Sex: Differences observed in metabolic rate
        - Environmental stimuli: Influence energy requirements

  • Diet Composition Influence on TEF:
        - Varies based on macronutrient intake

  • Obesity and Insulin Resistance:
        - Can affect BMR and overall energy dynamics. Generally, BMR accounts for 60-75% of TEE.

Energy Balance

  • Definition:
      - The relationship can be expressed as:

    • Energy intake - energy expenditure = change in body mass (new tissue / energy stores)
        - Positive energy balance during growth is important to allow for body growth but must avoid excessive adiposity (fat accumulation).
        - Most adults target zero energy balance, maintaining stable body weight over long periods.
        - Individuals typically adjust their energy intake in response to fluctuations in energy requirements.

Regulation of Energy Intake

  • Leptin:
      - Description: The primary hormone signaling energy stores
      - Origin: Secreted by adipose tissues
      - Relationship: Levels increase with body fat; also informs the body of energy balance.

  • Insulin:
      - Basal insulin levels indicate overall energy status. Plasma insulin changes also respond to short-term variations in energy intake, affecting satiety signals.

  • Ghrelin:
      - Description: A gut hormone that stimulates appetite
      - Mechanism: Produced by stomach cells when empty, signaling hunger.

  • Impact on Central Melanocortin System:
      - Both leptin/insulin and ghrelin modify activity within the hypothalamic melanocortin system. The melanocortin system involves neurons that regulate energy intake based on signals.

Hypothalamic Regulation and Neuronal Activity

  • Neuronal Interactions:
      - Interaction of hormones like ghrelin, insulin, and leptin with neurons in the hypothalamus leads to stimulation or inhibition of feeding.
      - The Paraventricular Nucleus (PVN) houses neurons that integrate these signals to affect food intake.
        - Specific pathways: MCR-4 receptors and AGRP/NPY neurons relate to appetite stimulation, while POMC/CART neurons play a role in food intake inhibition.

  • GLP-1 also acts on neurons, specifically targeting the hypothalamus to enhance satiety and reduce food intake, thereby influencing overall energy balance.

  • Cholecystokinin (CCK) interacts with CCK receptors in the brain, particularly within the hypothalamus, to promote satiety and limit food consumption. This hormone is released in response to food intake and signals fullness, thereby modulating neuronal activity to decrease appetite and support energy balance.

Leptin and Obesity

  • Discovery of the ob/ob Gene:
      - Year: 1950, Jackson laboratory identified a mutation (ob/ob) in mice that leads to excessive eating and obesity.
      - 1990 Research:
        - Scientists Leibel and Friedman mapped the ob gene. This gene encodes leptin which acts as an appetite suppressor.

Leptin Regulation of Fat Stores

  • Diagrammatic representation suggests that:
      - High Secretion of Leptin: Indicates increased adipose tissue, promotes reduced energy intake, and may enhance energy expenditure.
      - Low Secretion of Leptin: Corresponds with decreased adipose tissue, signals a potential need for increased energy intake and may reduce energy expenditure.

Congenital Leptin Deficiency

  • Outcomes of normalization include
      - Appetite control
      - Reduction in fat mass
      - Impact on plasma insulin, plasma lipids, thyroid hormones, and gonadotropins/puberty.
      - Reference DOI: http://dx.doi.org/10.1172/JCI15693

Misconception about Obesity and Leptin

  • Findings:
      - While leptin resistance occurs, obese individuals are not necessarily deficient in leptin.

  • Question Raised:
      - What are the underlying causes of obesity if not solely leptin deficiency?