Table 1.

Overview of the most dominant hormonal changes in systemic inflammation and their contribution to the observed metabolic changes. Upward arrows symbolize “upregualation”, downward arrows symbolize “downregulation”.

Hormone	Pathway	Metabolic Changes
Increased
Cortisol	−binding to the glucocorticoid receptor in the nucleus → expression of enzymes involved in gluconeogenesis ↑ and β2-adreno receptors ↑ and further anti-inflammatory proteins (e.g., lipocortin, Interleukin-1-Receptor Antagonist (IL-1RA), I κB Kinase) −inhibition of transcription of nuclear factor κ B (NFκB)-dependent genes	−gluconeogenesis ↑ in hepatocytes −lipolysis ↑ proteolysis ↑
Nor-/Epinephrine	−via β2-receptors (cAMP ↑) in liver and skeletal muscle −via β3-Receptors (cAMP ↑) in adipocytes	−lipolysis ↑ and gluconeogenesis ↑ in liver and skeletal muscle. −lipolysis ↑ and ketogenesis ↑ in adipocytes
Vasopressin	−via V1-receptors	−glycogenolysis ↑
Insulin (although its effects are impaired by peripheral insulin resistance)	−binding to the insulin receptor → activation and deactivation of enzymes via kinase cascades involving phosphoinositid-3-kinase, the PI3-cascade and the activation of protein kinase B (PKB).	In hepatocytes and skeletal muscle −insertion of glucose transporter type 4 (GLUT4) molecules into the cell membranes of adipocytes and skeletal muscles −glycogen synthesis ↑ −gluconeogenesis ↓ −triglyceride synthesis ↑ −lipolysis ↓ −cell growth ↑ −cell proliferation ↑ −autophagy ↓
Glucagon	−binding to G protein-coupled receptors− → cAMP ↑ → protein kinase A activity ↑	−glycogenolysis ↑
Reduced
Thyroid-stimulating hormone (TSH) ↓, triiodothyronine (T3) ↓, thyroxine (T4) ↓	−changes of gene expression	−insertion of β-adreno receptors in cell membranes ↓ −insertion of α-adreno receptors in cell membranes ↑ −insulin secretion ↓ −corticosteroid and catecholamine production and secretion ↓