Energy Metabolism and Temperature Regulation

• Tissue: Aggregate of differentiated cells with similar properties (major tissues: muscle, nervous, epithelial, connective).
• Organ: The presence of two or more distinct tissues that work together for one or more common functions (examples: stomach, bladder, heart).
• the adipose tissue is considered part of the connective tissue.
• Parenchymal adipocytes

  A) adiposcytes

  B) stored lipids

  C) nucleus and cytoplasm

  
• The adipose organ: several cell types that interact to coordinate the metabolic functions.

  Adipocytes and their stem/progenitor cells.

  Vascularized by blood & lymphatic vessels.

  Innervated by sympathetic & sensory nerves.

  Immune cells (adipose inflammation, insulin sensitivity)

  Fibroblasts (adipose fibrosis in obesity)

  Mesothelial cells (a layer of epithelial cells lining visceral fat)
• two major depots of distribution of white adipose depots: visceral and subcutaneous
• Visceral: intra-abdominal, surrounding organs

  Retroperitoneal: behind the peritoneumOmental: originating at the stomach and draping the intestinesMesenteric: holding the intestines in their loop structurePericardialPerirenal
• Subcutaneous: under the skin
• white adipose depots in other organs: dermal adipose, bone marrow, adipose, mammary adipose
• how to make an adipocyte:

  1. Adipogenesis
  2. De novo Lipogenesis
  3. Triglycerol synthesis
• adipogenesis: genereates new fat cells from stem cells
• Mesenchymal stem cells are multi-potent, adult progenitor cells that are also capable of forming myoblasts, osteoblasts and chondroblasts. They reside in the adipose organ
• Preadipocytes are committed, uni-potent, fibroblast-like progenitors of adipocytes.
• The differentiation of adipocytes requires hormones such as insulin and is controlled by a network of transcriptional factors (i.e., PPAR gamma).
• adipocyte

  A) mesenchymal stem cell

  B) commitment

  C) preadipocyte

  D) differentiation

  E) mature adipocyte

  
• De novo Lipogenesis (DNL): converts excesscarbohydrate into fatty acids

  • Glucose uptake & glycolysis

  • Pentose phosphate pathway

  • Fatty acid synthesis

  • Although observed in adipocytes, DNL mostlytakes place in the liver and fat is secreted as very low density lipoprotein (VLDL)
• Triacylglycerol synthesis: esterification of fattyacids to glycerol

  • Fatty acid uptake FA from food, DNL in the liver, and DNL in adipocytes

  • TAG synthesis
• how to make lipids that fill up the adipocyte (de novo Lipogenesis)

  A) glucose uptake

  B) glycolysis

  C) pentose phosphate pathway

  D) fatty acid synthesis

  E) fatty acid uptake

  F) fatty acid uptake

  G) TAG synthesis

  
• Functions of the white adipose organ:

  1. energy storage
  2. endocrine function
• Energy storage

  • Nearly the entire volume of each adipocyte is occupiedby a lipid droplet (dominated by triacylglycerol).

  • Lipids are the most concentrated form of energystorage and they major expendable fuel source.

  • Food availability is irregular, fat storage allows for greater mobility and promotes survival during famine.
• body fatness is evolutionarily selected
• fat storage is a widely observed phenomenon, from worms to humans
• Fat storage serves as a reserve for unanticipatedshortfalls in food supply.

  • Animals cannot switch off energy demands.
  • Limited glycogen/glucosereserve.
  • Individuals storing more fatcan survive longer duringstarvation.
• Thrifty gene hypothesis: under conditions of uncertain food supply, genes promoting fat storage will be positively selected
• If the avoidance of starvation was the only criterion, one would predict thatindividuals should maximize their fat storage levels
• Fat storage also brings disadvantages, the most conspicuous of which is the risk of predation.

  • Less agile; lower maximal speeds to evade; longer foraging and thus more likely to be predated
• with lower body fatness, you have increased risk of starvation and mechanisms enabled to increase fatness
• with high body fatness, you have increased risk of predation and mechanisms enabled to decrease fatness
• Body mass index (BMI): [weight in kg]/[height in meters]^2

  • Healthy: 18.5 - 24.9; Overweight: 25 - 29.9; Obese: > 30; Extremely obese: > 40.
  • Factors such as age, sex, ethnicity, and muscle mass can influence the relationshipbetween BMI and body fat.
  • BMI does not distinguish between excess fat or muscle, nor does it provide anyindication of the distribution of fat.
• Low WHR (subcutaneous or pear-shaped obesity) are at low risk for metabolic complications of obesity
• High WHR (visceral or apple-shaped obesity) are at high risk for these complications.
• Fat distribution can be estimated by the waist to hip ratio (WHR).
• lipid overflow-ectopic fat model

  A) normal metabolic profile

  B) no ectopic fat

  C) abscence of metabolic syndrome clinical criteria

  D) altered metabolic profile

  E) presence of metabolic syndrome clinical criteria

  
• types of adipose expansion during obesity:

  1. hyperplasic adipose expansion
  2. hypertrophic adipose expansion
• Hyperplasic adipose expansion

  • Increased adipocyte number
  • Predominantly in subcutaneous fatand premenopausal women.
  • Linked to beneficial phenomena
  • decreased fatty acids release, pro-inflammatory cytokine release,immune cell recruitment, hypoxia,fibrosis
  • improved insulin sensitivity