Acute high-fat feeding leads to disruptions in glucose homeostasis and worsens stroke outcome

J Cereb Blood Flow Metab. 2019 Jun;39(6):1026-1037. doi: 10.1177/0271678X17744718. Epub 2017 Nov 24.

Abstract

Chronic consumption of diets high in fat leads to obesity and can negatively affect brain function. Rodents made obese by long-term maintenance on a high-fat diet have worse outcome after experimental stroke. High-fat consumption for only three days does not induce obesity but has rapid effects on the brain including memory impairment. However, the effect of brief periods of high-fat feeding or high-fat consumption in the absence of obesity on stroke is unknown. We therefore tested the effect of an acute period of high-fat feeding (three days) in C57B/6 mice on outcome after middle cerebral artery occlusion (MCAo). In contrast to a chronic high-fat diet (7.5 months), an acute high-fat diet had no effect on body weight, adipose tissue, lipid profile or inflammatory markers (in periphery and the brain). Three days of high-fat feeding impaired glucose tolerance, increased plasma glucose and insulin and brain expression of the glucose transporter GLUT-1. Ischaemic damage was increased (48%) in mice fed an acute high-fat diet, and was associated with a further reduction in GLUT-1 in the ischaemic hemisphere. These data demonstrate that only a brief period of high-fat consumption has a negative effect on glucose homeostasis and worsens outcome after ischaemic stroke.

Keywords: Brain ischaemia; glucose; high-fat diet; hyperglycemia; inflammation; lipids; stroke.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism*
  • Diet, High-Fat / adverse effects*
  • Glucose Intolerance
  • Glucose Transporter Type 1 / metabolism
  • Homeostasis*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Stroke / pathology*
  • Time Factors

Substances

  • Blood Glucose
  • Glucose Transporter Type 1
  • Slc2a1 protein, mouse