Epidemiological and experimental links between air pollution and type 2 diabetes
Liu C., Ying Z., Harkema J., Sun Q., Rajagopalan S.
Narrative Review on Type 2 Diabetes, Chronic Inflammation, published in Toxicol Pathol (2013) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Toxicol Pathol (2013)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 23104765
- PMCID
- PMC3988529
- DOI
- 10.1177/0192623312464531
- Citations
- 111
Abstract (original English)
There is increasing evidence suggesting links between exposure to environmental toxins and susceptibility to type 2 diabetes mellitus (DM). In this review, we summarize the experimental evidence to support this association that has been noted in many epidemiologic studies. Inflammation in response to particulate matter (PM(2.5)) exposure in air pollution represents a common mechanism that may interact with other pro-inflammatory influences in diet and life style to modulate susceptibility to cardiometabolic diseases. The role of innate immune cytokines released from macrophages in the lung is well known. In addition, chemokine triggers in response to air-pollution exposure may mediate a cellular response from the bone marrow/spleen through toll-like receptors (TLRs) and Nucleotide Oligomerization Domain receptors (NLRs) pathways to mediate inflammatory response in organs. Emerging data also seem to support a role for PM(2.5) exposure in endoplasmic reticulum stress-induced apoptosis and in brown adipose tissue dysfunction. Decreased expression of UCP1 in brown adipose tissue may account for reduced thermogenesis providing another link between PM(2.5) and insulin resistance. The implications of an experimental link between air-pollution exposure and type 2 DM are profound as air pollution is a pervasive risk factor throughout the world and even modest alleviation in exposure may
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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