IMPAIRED GLUCOSE METABOLISM

EXCESS CORTISOL IMPAIRS NORMAL GLUCOSE METABOLISM AND HOMEOSTASIS

Glucocorticoid excess can impair normal glucose metabolism and homeostasis through many different mechanisms, leading to impaired fasting glucose, impaired glucose tolerance, and hyperglycemia.1

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HYPERGLYCEMIA DRIVEN BY HYPERCORTISOLISM

Hyperglycemia results from a combination of systemic dysfunctions, known as the “ominous octet.” Excess cortisol can cause dysfunction in 7 of the 8 systems, which can lead to hyperglycemia and type 2 diabetes (T2D).1-3

Effect of elevated cortisol on cells and tissues

Pancreas icon depicting beta cell.

β CELL1

  • Impaired β-cell activity
  • Increased β-cell apoptosis
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LIVER1,3,4

Increased

  • Gluconeogenesis
  • Glycogenolysis
  • Hepatic glucose output
  • Glucagon secretion

Decreased

  • Glycogen synthesis
  • Insulin sensitivity
Brain icon.

BRAIN1

  • Circadian disruption of metabolism regulation
  • Neuropeptide secretion
  • Increased catecholamine signaling
Fat cells icon.

FAT CELLS1

  • Increased lipolysis
  • Increased substrates for gluconeogenesis
  • Increased fatty acid levels
  • Increased fat deposition
Alpha cell icon.

α CELL1

  • Increased glucagon secretion
Muscle icon.

MUSCLE1,4

Increased

  • Proteolysis
  • Substrates for gluconeogenesis

Decreased

  • Glucose uptake
  • Glycogen synthesis
Gut icon.

GUT1

  • Decreased incretin secretion
  • Decreased GLP-1 secretion
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Up to 10% of patients with difficult-to-control T2D may have hypercortisolism5-7

UNCOVER PREVALENCE
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Hypercortisolism can lead to worsening T2D8

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References

1. Scaroni C, Zilio M, Foti M, Boscaro M. Endocr Rev. 2017;38(3):189-219. doi:10.1210/er.2016-1105 2. Defronzo RA. Banting Lecture. Diabetes. 2009;58(4):773-795. doi:10.2337/db09-9028 3. Barbot M, Ceccato F, Scaroni C. Front Endocrinol (Lausanne). 2018;9:284. doi:10.3389/fendo.2018.00284 4. Pivonello R, De Leo M, Vitale P, et al. Neuroendocrinology. 2010;92(suppl 1):77-81. doi:10.1159/000314319 5. Chiodini I, Torlontano M, Scillitani A, et al. Eur J Endocrinol. 2005;153(6):837-844. doi:10.1530/eje.1.02045 6. Catargi B, Rigalleau V, Poussin A, et al. J Clin Endocrinol Metab. 2003;88(12):5808-5813. doi:10.1210/jc.2003-030254 7. Costa DS, Conceição FL, Leite NC, Ferreira MT, Salles GF, Cardoso CR. J Diabetes Complications. 2016;30(6):1032-1038. doi:10.1016/j.jdiacomp.2016.05.006 8. Elhassan YS, Alahdab F, Prete A, et al. Ann Intern Med. 2019;171(2):107-116. doi:10.7326/M18-3630