Table 1.

Associations of AFABP with cardiometabolic conditions.

	Circulating AFABP level	Potential mechanistic actions	References
Type 2 diabetes	Predicts the development of type 2 diabetes	Increases free fatty acid efflux Reduces glucose utilization in muscles Increases hepatic expression of gluconeogenic enzymes	(25, 47–51)
Hypertension	Correlates positively with blood pressure	Increases endothelial dysfunction Worsens insulin sensitivity	(47, 48, 50, 52)
Dyslipidemia	Correlates positively with low-density lipoprotein cholesterol Correlates negatively with high-density lipoprotein cholesterol	Increases free fatty acid efflux Negative effects on lipid metabolism Worsens insulin sensitivity	(47, 48, 50)
Coronary heart disease	Predicts the development of cardiovascular diseases Associates with coronary calcium score in patients with type 2 diabetes Associates with the coronary plaque burden in patients with coronary heart disease	Promotes atherosclerosis development: Alters lipid metabolism in macrophages and facilitates foam cell formation Promotes saturated fatty acid-induced ceramide production in macrophages Mediates toxic lipids-induced endoplasmic reticulum stress in macrophages Increases adipose tissue and systemic inflammation	(33, 53–60)
Stroke	Associates with the presence of carotid atherosclerosis Correlates positively with the vulnerable carotid plaque phenotype Doubles the risk of incident adverse cardiovascular events including cardiovascular mortality, non-fatal myocardial infarction and non-fatal stroke. Predicts poor functional outcome and mortality from ischemic stroke	Promotes atherosclerosis development (as above) Enhances the production of matrix metalloproteinases-9 which degrade the tight junction proteins in the blood brain barrier, leading to cerebral edema, increased neuro-inflammation and poor neurological outcomes	(61–68)
Heart failure	Correlates positively with circulating levels of N-terminal fragment of pro-B-type natriuretic peptide Associates with the presence of left ventricular systolic and/or diastolic dysfunction Associates with increasing severity of clinical heart failure Predicts incident heart failure among older individuals	Negative inotropic effect on cardiomyocytes Reduces phosphorylation of endothelial nitric oxide synthase in acute myocardial ischemia/reperfusion injury Increases oxidative stress and cardiac inflammation Increases cardiac hypertrophy and fibrosis	(52, 69–75)
Cardiovascular mortality	Associates with both short- and long-term cardiovascular morbidity and mortality in patients with established coronary heart disease Predicts cardiovascular deaths in patients with type 2 diabetes	See above	(76–80)