Obesity-induced dysbiosis in the gut is usually marked by a reduced expression of the gut junction proteins ZO-1 and occludin which in turn leads to increased serum lipopolysaccharide (LPS) through a ‘leaky gut’ membrane [106], and the resulting low-grade systemic inflammation and activated pro-inflammatory cytokines have the potential of affecting the BBB and triggering neuroinflammation in vital brain parts, particularly the hippocampus and the amygdala [107,108]. The gene discussed is OCLN; the disease is obesity due to melanocortin 4 receptor deficiency.