Adipocyte-Derived CCHamide-1 , Eiger , Growth-Blocking Peptide 3 , and Unpaired 2 Regulate Drosophila melanogaster Oogenesis.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

In addition to energy storage, adipose tissue communication to other organs plays a key role in regulating organismal physiology. While the link between adipose tissue dysfunction and pathophysiology, including diabetes, chronic inflammation, and infertility, is clear, the molecular mechanisms that underlie these associations have not been fully described. We use Drosophila melanogaster as a model to better understand how adipose tissue communicates to the ovary. In this study, we utilized D. melanogaster's robust genetic toolkit to examine the role of five adipokines known to control larval growth during development, CCHamide-1 , CCHamide-2 , eiger , Growth-blocking peptide 3 , and unpaired 2 in regulating oogenesis. We show that the adult fat body expresses these "larval" adipokines. Our data indicate that ovarian germline stem cell maintenance does not require these adipokines. However, adipocyte-derived CCHamide-1 , eiger , Growth-blocking peptide 3 , and unpaired 2 influence early and late germline survival as well as ovulation. Thus, this work uncovers several adipokines that mediate fat-to-ovary communication.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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