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Lecture 21

BIOCHEM 4M03 Lecture Notes - Lecture 21: Mast Cell Stabilizer, White Adipose Tissue, Ketotifen

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Deborah Sloboda

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Biochem 4M04 Lecture 21 Journal Club: Interplay between Macrophages & Mast Cells
in Metabolic Disease
- Leptin Deficiency Shifts Mast Cells toward Anti-inflammatory Actions and Protects Mice
from Obesity and Diabetes by Polarizing M2 Macrophages
Last Journal Club
- White adipose Tissue Low-Grade Inflammation in TPH1+/+ and TPH-/-
- TPH-/- leaner
- Decrease in inflammatory markers these markers are all associated with
- CD69 macrophage specific cell surface glycoprotein
- Can induce proinflamatory environment
Immunity & Metabolism
- Nutrient excess in interplay of these 3 cells: mast cells, macrophages, eosinophils
- TPH1 is rate limiting enzyme of serotonin specifically in periphery nervous system
- Cytokines: substances secreted by immune cells that have effects on other cells (ex.
- Eosinophils induce M2 macrophages
- Both eosinophils and M2 macrophages can modulate shift of PDGFR-alpha
mesenchymal cells
- Eosinophils go to IL-4 (interleukin-4induce mesenchymal cells)
- Ex. Beige Adipose Tissue
Macrophages & Obesity
- In lean individuals, not as many macrophages
- Increase in body weight in mice, increase CD68 expression, increase BMI
- Increase in average adipocyte area with nutrition excess, increase in F4/80 (main
histology marker)
- Obesity is associated with macrophage accumulation in adipose tissue
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Macrophage Polarization
- M1: Genes associated iNOS, TNFalpha, IL6
- M1 macrophage polarization
o Secrete TNF andIL-1 beta, inhibit insulin sensitivity
More glucose and fat deposition in bloodstream T2D, hyperglycemia,
o Secrete MCP1 (CCL2)
o M1 macrophages induce proinflammatory state that fosters obese adipose tissue
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