Chronic Stress and Diabetes Mellitus: Interwoven Pathologies.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms without systematic methodology or primary human empirical data.
PubMed 31713487 · doi:10.2174/1573399815666191111152248
What was done
This narrative review summarizes the neuroendocrine mechanisms connecting chronic stress, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and the development of Type 2 diabetes (T2D).
What was found
No quantitative findings or empirical metrics were reported in the abstract. The authors describe the biological cascade wherein chronic stress causes HPA axis dishabituation and sustained secretion of glucocorticoids and catecholamines, which promote hepatic gluconeogenesis, suppress glucose uptake in muscle and adipose tissue, promote lipolysis, inhibit insulin secretion, and induce insulin resistance and inflammation.
Why it matters
Understanding the neuroendocrine links between stress hormones and metabolic dysfunction clarifies how prolonged stress contributes to diabetes pathogenesis and highlights glucocorticoid pathway regulation as a potential therapeutic target.
Limits
The abstract describes a narrative conceptual framework without systematic search methodology, quantitative effect sizes, primary human sample sizes, or clinical trial evidence.
Cited by
- supports Chronic stress is directly associated with insulin resistance.