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Review
. 2017 Jul;19(4):921-930.
doi: 10.1208/s12248-017-0079-3. Epub 2017 Apr 10.

Blood-Brain Barriers in Obesity

Elizabeth M Rhea  1   2 , Therese S Salameh  3   4 , Aric F Logsdon  3   4 , Angela J Hanson  3   4 , Michelle A Erickson  3   4 , William A Banks  3   4
Affiliations
Review

Blood-Brain Barriers in Obesity

Elizabeth M Rhea et al. AAPS J. 2017 Jul.

Abstract

After decades of rapid increase, the rate of obesity in adults in the USA is beginning to slow and the rate of childhood obesity is stabilizing. Despite these improvements, the obesity epidemic continues to be a major health and financial burden. Obesity is associated with serious negative health outcomes such as cardiovascular disease, type II diabetes, and, more recently, cognitive decline and various neurodegenerative dementias such as Alzheimer's disease. In the past decade, major advancements have contributed to the understanding of the role of the central nervous system (CNS) in the development of obesity and how peripheral hormonal signals modulate CNS regulation of energy homeostasis. In this article, we address how obesity affects the structure and function of the blood-brain barrier (BBB), the impact of obesity on Alzheimer's disease, the effects of obesity on circulating proteins and their transport into the brain, and how these changes can potentially be reversed by weight loss.

Keywords: blood-brain barrier; insulin; leptin; obesity.

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Figures

Fig. 1
Fig. 1
Changes at the BBB in obesity. The BBB is exposed to increased circulating levels of leptin, insulin, free fatty acids, and the cytokines IL-6 and TNF-α, whereas ghrelin and adiponectin levels are decreased in obesity (black vertical arrows). The blood-to-brain transport of leptin, insulin, and ghrelin (blue arrows) is decreased and transport of free fatty acids (FFA, purple arrow) is increased in obesity. Triglycerides (TG) can also decrease leptin transport while increasing insulin and ghrelin transport (horizontal arrows). Obesity decreases mRNA levels of P-glycoprotein (P-gp) in BBB endothelial cells. The obesity-associated decrease in circulating adiponectin stimulates the abluminal secretion of IL-6 by BBB endothelial cells, resulting in increased brain IL-6 levels
Fig. 2
Fig. 2
Effects of obesity reversal on BBB transport, CNS inflammation, and metabolic mediators. Obesity reversal results in many metabolic improvements including improvements in insulin resistance. These improvements extend to the CNS in which transport of peripheral peptides across the BBB is restored and inflammation is decreased, not only in the periphery but also in the CNS. Other weight loss interventions such as exercise, bariatric surgery, and pharmaceutical therapies could also exhibit similar effects on the BBB in restoring the connection between the periphery and the CNS
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