Transposable elements (TEs) are mobile sequences of DNA that parasitize the genomes of their hosts. Due to their replicative ability, TEs account for large portions of their host genomes including nearly 30% of the fly genome and 45% of the human genome. To combat the invasion and expansion of TEs, small RNA (smRNA) silencing pathways have evolved to suppress TEs across species from plants to humans. Such pathways are essential in maintaining genomic integrity by preventing TE transposition that could disrupt normal gene function in otherwise healthy tissues. The Piwi-interacting (piRNA) pathway, classically associated with gonadal tissues, employs 23-29nt smRNAs complexed with argonaute proteins to actively suppress TEs in the germline of animals. However, recent evidence has begun to suggest that components of this pathway may in fact be present in somatic tissues of multiple species including flies, mice, monkeys, and humans. Here we provide evidence of a functional somatic piRNA pathway in the adult Drosophila abdominal fat body including the presence of the piRNA effector protein Piwi and canonical 23-29nt long piRNAs that map to TEs and piRNA clusters known to produce TE piRNAs. We also observed fat body genic piRNAs that map to 3’UTRs, another known source of piRNAs in the gonads. piwi mutants exhibit depletion of both TE- and 3’UTR-mapping piRNAs, increased TE transcript levels, TE transposition in the fat body, altered metabolic gene expression, and reduced lipid and glycogen reserves. Finally, piwi mutants are also sensitive to starvation, immunologically compromised, and have shortened lifespans, all hallmarks of compromised tissue function in the fat body. These findings demonstrate the presence of a functional non-gonadal somatic piRNA pathway in the adult fat body that impacts normal metabolism, immunological function, and overall organismal health.