dSec16 Acting in Insulin-like Peptide Producing Cells Controls Energy Homeostasis in Drosophila .
Ruo-Xin ZhangSha-Sha LiAn-Qi LiZhi-Ying LiuG Gregory NeelyG Gregory NeelyPublished in: Life (Basel, Switzerland) (2022)
Many studies show that genetics play a major contribution to the onset of obesity. Human genome-wide association studies (GWASs) have identified hundreds of genes that are associated with obesity. However, the majority of them have not been functionally validated. SEC16B has been identified in multiple obesity GWASs but its physiological role in energy homeostasis remains unknown. Here, we use Drosophila to determine the physiological functions of dSec16 in energy metabolism. Our results showed that global RNAi of dSec16 increased food intake and triglyceride (TAG) levels. Furthermore, this TAG increase was observed in flies with a specific RNAi of dSec16 in insulin-like peptide producing cells (IPCs) with an alteration of endocrine peptides. Together, our study demonstrates that dSec16 acting in IPCs controls energy balance and advances the molecular understanding of obesity.
Keyphrases
- type diabetes
- insulin resistance
- metabolic syndrome
- weight loss
- high fat diet induced
- induced apoptosis
- weight gain
- cell cycle arrest
- glycemic control
- adipose tissue
- endoplasmic reticulum stress
- skeletal muscle
- gene expression
- oxidative stress
- cell death
- dna methylation
- cell proliferation
- physical activity
- pi k akt
- transcription factor