The role of monoaminergic neurotransmission for metabolic control in the fruit fly drosophila melanogaster

TY - JOUR

T1 - The role of monoaminergic neurotransmission for metabolic control in the fruit fly drosophila melanogaster

AU - Li, Yong

AU - Tiedemann, Lasse

AU - Von Frieling, Jakob

AU - Nolte, Stella

AU - El-Kholy, Samar

AU - Stephano, Flora

AU - Gelhaus, Christoph

AU - Bruchhaus, Iris

AU - Fink, Christine

AU - Roeder, Thomas

PY - 2017/8/22

Y1 - 2017/8/22

N2 - Hormones control various metabolic traits comprising fat deposition or starvation resistance. Here we show that two invertebrate neurohormones, octopamine (OA) and tyramine (TA) as well as their associated receptors, had a major impact on these metabolic traits. Animals devoid of the monoamine OA develop a severe obesity phenotype. Using flies defective in the expression of receptors for OA and TA, we aimed to decipher the contributions of single receptors for these metabolic phenotypes. Whereas those animals impaired in octβ1r, octβ2r and tar1 share the obesity phenotype of OA-deficient (th-deficient) animals, the octβ1r, octβ2r deficient flies showed reduced insulin release, which is opposed to the situation found in th-deficient animals. On the other hand, OAMB deficient flies were leaner than controls, implying that the regulation of this phenotype is more complex than anticipated. Other phenotypes seen in th-deficient animals, such as the reduced ability to perform complex movements tasks can mainly be attributed to the octβ2r. Tissue-specific RNAi experiments revealed a very complex interorgan communication leading to the different metabolic phenotypes observed in OA or OA and TA-deficient flies.

AB - Hormones control various metabolic traits comprising fat deposition or starvation resistance. Here we show that two invertebrate neurohormones, octopamine (OA) and tyramine (TA) as well as their associated receptors, had a major impact on these metabolic traits. Animals devoid of the monoamine OA develop a severe obesity phenotype. Using flies defective in the expression of receptors for OA and TA, we aimed to decipher the contributions of single receptors for these metabolic phenotypes. Whereas those animals impaired in octβ1r, octβ2r and tar1 share the obesity phenotype of OA-deficient (th-deficient) animals, the octβ1r, octβ2r deficient flies showed reduced insulin release, which is opposed to the situation found in th-deficient animals. On the other hand, OAMB deficient flies were leaner than controls, implying that the regulation of this phenotype is more complex than anticipated. Other phenotypes seen in th-deficient animals, such as the reduced ability to perform complex movements tasks can mainly be attributed to the octβ2r. Tissue-specific RNAi experiments revealed a very complex interorgan communication leading to the different metabolic phenotypes observed in OA or OA and TA-deficient flies.

KW - Body fat distribution

KW - Insulin

KW - Insulin release

KW - Octopamine receptor

KW - Tyramine receptor

UR - http://www.scopus.com/inward/record.url?scp=85029226587&partnerID=8YFLogxK

U2 - 10.3389/fnsys.2017.00060

DO - 10.3389/fnsys.2017.00060

M3 - Journal article

C2 - 28878633

AN - SCOPUS:85029226587

SN - 1662-5137

VL - 11

JO - Frontiers in Systems Neuroscience

JF - Frontiers in Systems Neuroscience

M1 - 60

ER -