High fat diet and body weight have different effects on cannabinoid CB1 receptor expression in rat nodose ganglia

It has been already established that specific bidirectional, hormonal and neuronal pathways exist between the central nervous system (CNS) and the gastrointestinal tract, liver, pancreas, and adipose tissue, regulating numerous physiological mechanisms, energy balance included (1, 2).

Being mainly in charge of these communication pathways, the vagal nerve allows different enteric structures to be in contact with vagal afferent neurons, whose cell bodies locate in the nodose ganglia. It is believed that these neurons express certain plasticity during feeding and fasting.

Closely associated with these pathways, the endocannabinoid system occupies a role in the control of food intake. This process is mediated by cannabinoid CB1 receptors through the ganglia expression of the orexin-1 receptor (OX-1R). It is known that, when CB1 receptors are activated, feeding is induced, while their deactivation inhibits food intake (3, 4).

Due to diverse reports that show a link between cannabinoid CB1 receptors, energy balance, and diet-induced body weights, this study aimed to discover the role of these receptors in different states of body weight, diets, and feeding periods through its determination in the nodose ganglia of rats.

For this experiment, male Wistar rats were submitted to free access to tap water and randomly assigned to either standard laboratory chow or a high fat diet. In addition, some of them were randomly submitted to fasting periods for further results. After 11 weeks, the age-matched rats fed with a high fat diet were classified into diet-induced obese (DIO) rats (≥ 612 g) or diet-resistant (DR) rats (≤ 590 g). Some rats matched body weight (wmDR) but not age, being only fed with a chow diet. Rats were fed ad libitum or fasted during 24 h before being anesthetized and killed to remove the nodose ganglia for study.

Other subjects were fed chow or high fat diet for 4 weeks, which then were fasted for up to 24 h. These were killed at the end of the fasting periods to remove the nodose ganglia for study. Other rats who only were fed a high fat diet were fasted for 0, 6, 12, 24, 36, and 48 h before being killed to remove the nodose ganglia.

After diverse study techniques, the results were:

  • In chow-fed rats, although their CB1 receptors immunoreactivity was comparable between the ad libitum fed and those fasted for 24 h, more available receptors were found in 24 h fasted rats.
  • DIO, DR, and wmDR rats presented a significantly higher immunoreactivity when compared to chow-fed rats. DIO and DR rats maintained similar results after a 24 h fast, without being modified after 48 h of fasting, while wmDr rats showed an increase in CB1 immunoreactivity after 24 h of fasting.
  • CB1 cell profile in the nodose ganglia in rats fed with a high fat diet for 4 weeks and fasted for 24 h did not change.

The study showed that CB1 receptors immunoreactivity in the nodose ganglia is dependent on feeding status, increasing in animals with greater body weights and submitted to high fat diets. In addition, these levels are not modified during ad libitum or fasting periods. However, in lean, chow-fed animals, these levels reduced when ad libitum fed and increased after a 24 h fast.

These results confirm the role played by CB1 receptors in the maintenance of feeding and fasting-induced neurochemical mechanisms in the nodose ganglia. Although this study demonstrated pre-established mechanisms, further studies are needed to be performed to achieve a better understanding of CB1 receptors´ contribution to the stimulation of food intake and maintenance of obesity (3, 4).

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