Visceral fat endocannabinoid overproduction is associated with insulin resistance and tissue dysfunction in mice and humans

Visceral fat endocannabinoid overproduction is associated with insulin resistance and tissue dysfunction in mice and humans Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications. Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications. Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications. Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications. Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications. Insulin resistance and severe metabolic dysregulation of adipocytes—rather than total fat mass alone—drive depot-specific endocannabinoid overproduction. Visceral adipose tissue acts as a primary source for elevated systemic endocannabinoid levels in type 2 diabetes, presenting a target for tissue-specific cannabinoid receptor type 1 ($\text{CB}_1$) signaling therapies to alleviate downstream metabolic complications.