FIGURE 4.

Diagrammatic depiction of the potential centrally mediated effects of increased leptin and resistin synthesis due to increased adiposity. Leptin and insulin can act in the brain to influence metabolic and cardiovascular outputs. Leptin elevates sympathetic nerve activity to the kidneys (RSNA), vasculature and to brown adipose tissue (BAT SNA). It also dramatically reduces food intake, body mass and decreases insulin secretion from the pancreas through actions in the brain. Resistin can act in the brain to increase sympathetic nerve activity to the kidneys and vasculature, but it decreases sympathetic nerve activity to brown adipose tissue. Resistin by acting in the brain increases insulin secretion and reduces food intake acutely (though less than leptin) and has little effect chronically. Thus, crosstalk within the brain between these two hormones could result in less thermogenesis (energy expenditure), a reduced anorexigenic effect, less insulin secretion but enhanced sympathetic nerve activity to the kidneys (and vasculature?) compared to the actions of leptin alone. This would result in increased metabolic and cardiovascular complications in conditions in which there is increased leptin and resistin. Black arrows signify direction and relative magnitude of change.