Modulation of metabolic hormone signaling<i>via</i>a circadian hormone and a biogenic amine in<i>Drosophila melanogaster</i>

Braco, Jason T.; Saunders, Cecil J.; Nelson, Jonathan M.; Johnson, Erik C.

doi:10.1101/2020.09.25.312967

Cited by 7 publications

(15 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This suggests that a common regulatory theme in these metabolic networks is that hormones that regulate APCs are likely to regulate IPCs as well and vice versa. Along those lines, we recently reported that the circadian hormone, PDF, modulates APCs [ 99 ] and previous descriptions have found this peptide also targets IPCs [ 100 ]. However, the above finding suggests that endocrine and intracellular metabolic context presumably is an important aspect that governs AKH release.…”

Section: Akh Receptor Distribution and Signalingmentioning

confidence: 84%

The Intrinsic Nutrient Sensing Adipokinetic Hormone Producing Cells Function in Modulation of Metabolism, Activity, and Stress

Nelson

Saunders

Johnson

2021

IJMS

Self Cite

View full text Add to dashboard Cite

All organisms confront the challenges of maintaining metabolic homeostasis in light of both variabilities in nutrient supplies and energetic costs of different physiologies and behaviors. While all cells are nutrient sensitive, only relative few cells within Metazoans are nutrient sensing cells. Nutrient sensing cells organize systemic behavioral and physiological responses to changing metabolic states. One group of cells present in the arthropods, is the adipokinetic hormone producing cells (APCs). APCs possess intrinsic nutrient sensors and receive contextual information regarding metabolic state through other endocrine connections. APCs express receptors for different hormones which modulate APC physiology and the secretion of the adipokinetic hormone (AKH). APCs are functionally similar to alpha cells in the mammalian pancreas and display a similar physiological organization. AKH release results in both hypertrehalosemia and hyperlipidemia through high affinity binding to the AKH receptor (AKHR). Another hallmark of AKH signaling is heightened locomotor activity, which accompanies starvation and is thought to enhance foraging. In this review, we discuss mechanisms of nutrient sensing and modulation of AKH release. Additionally, we compare the organization of AKH/AKHR signaling in different taxa. Lastly, we consider the signals that APCs integrate as well as recent experimental results that have expanded the functional repertoire of AKH signaling, further establishing this as both a metabolic and stress hormone.

show abstract

Section: Akh Receptor Distribution and Signalingmentioning

confidence: 84%

The Intrinsic Nutrient Sensing Adipokinetic Hormone Producing Cells Function in Modulation of Metabolism, Activity, and Stress

Nelson

Saunders

Johnson

2021

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…Yet, AKH appears to be one of presumably several factors that fine-tune locomotor activity patterns to meet physiological requirements under dietary stress-free conditions. OANs and APCs receive a multitude of converging and interconnected inputs, especially from insulin-producing cells (IPCs), with extensive feedbacks (see [70][71][72]). For example, OANs in the SEZ express receptors for AKH and DILPs, and integrate the nutritional status by responding to AKH and DILPs in an antagonistic fashion [9].…”

Section: Discussionmentioning

confidence: 99%

“…For example, OANs in the SEZ express receptors for AKH and DILPs, and integrate the nutritional status by responding to AKH and DILPs in an antagonistic fashion [9]. In turn, APCs express a range of OA receptors [72]. In addition, APCs are negatively modulated by insulin-producing cells (IPCs), suggesting feedforward signalling from IPCs to OANs via AKH signalling in parallel to direct IPC:OAN signalling [72,73].…”

Section: Discussionmentioning

confidence: 99%

“…In turn, APCs express a range of OA receptors [72]. In addition, APCs are negatively modulated by insulin-producing cells (IPCs), suggesting feedforward signalling from IPCs to OANs via AKH signalling in parallel to direct IPC:OAN signalling [72,73]. AKH signalling is also required for the carbohydratedependent release of DILP3 [74], and represses expression of DILP2,3 and 5 [71].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Endocrine fine-tuning of daily locomotor activity patterns under non-starving conditions in Drosophila

Pauls

Selcho

Raederscheidt

et al. 2020

Preprint

View full text Add to dashboard Cite

body ATP-sensitive potassium channels [6]. This triggers AKH release in a calcium-and AMP-activated protein kinase-dependent fashion [13]. Similar to glucagon, AKH acts on energy stores in the fat body by mobilising carbohydrates in form of the haemolymph sugar trehalose (hypertrehalosaemic effect), and by mobilising lipid depots (adipokinetic effect) [8,[14][15][16].OA, an analogue to vertebrate noradrenaline, is considered to act as an insect stress or arousal hormone [17]. OA is produced by octopaminergic neurons (OANs) located mostly along the midline in the brain and ventral nerve cord [18]. Among other functions, OA exerts myotropic effects on skeletal muscles [19] and mediates the adaptation of muscle metabolism to the physiological demands of locomotion [20][21][22].Both AKH and OA are crucial for starvation-induced hyperactivity, as this behaviour is absent in flies with impaired AKH or OA signalling [4,5,[7][8][9]. AKH activates a subset of OANs which are required for starvation-induced hyperactivity [5,9]. These neurons express receptors for AKH and Drosophila insulin-like peptides (DILPs). DILPs act antagonistically to AKH, and suppress starvation-induced hyperactivity via the OANs [9]. Yu and colleagues (2016) showed that the AKH-dependent increase in locomotor activity upon starvation represents a neuromodulatory and behavioural role of AKH and is not an indirect consequence of altered energy metabolism.Remarkably, studies in various insect species suggest that AKH and also OA play a role in the regulation of locomotor activity when the insects have free access to food (reviewed in [23]). For example, the circulating haemolymph titres of AKH correlate positively with daily rhythms in walking activity in the linden bug Pyrrhocoris apterus [24,25]. In Pyrrhocoris [26,27], crickets [28] and the cockroach Periplaneta americana [29,30], injection into the haemolymph or topical application of AKH induces a strong increase in locomotor activity in ad libitum fed animals, independent of the time of day [27,29]. Also in Drosophila, genetic overexpression of AKH enhances locomotor activity when food is freely available [31]. Unlike for starvation-induced hyperactivity, however, it is unclear whether and how AKH:OAN signalling contributes to shape daily activity under ad libitum feeding conditions, or whether increased AKH signalling is a consequence of a locomotor-induced increase in energy demands. Cockroach AKHs are known to increase the spontaneous neuronal activity of octopaminergic dorsal unpaired median neurons in the central nervous system, which express a

show abstract

“…11b). Therefore, based on these results and those of a previous RNA-seq analysis 39 , we surmised that NPFR is expressed in the CC. Since the CC produces the glucagon-like peptide, AKH, which regulates organismal carbohydrate and triglyceride metabolism in insects 2,20,40–42 , we were particularly interested in examining whether NPFR in the CC is involved in metabolic regulation in adult D. melanogaster .…”

Section: Resultsmentioning

confidence: 62%

The sugar-responsive enteroendocrine neuropeptide F regulates lipid metabolism through glucagon-like and insulin-like hormones inDrosophila melanogaster

Yoshinari

Kosakamoto

Kamiyama

et al. 2021

Preprint

View full text Add to dashboard Cite

The enteroendocrine cell (EEC)-derived incretins play a pivotal role in regulating the secretion of glucagon and insulins in mammals. Although glucagon-like and insulin-like hormones have been found across animal phyla, incretin-like EEC-derived hormones have not yet been characterised in invertebrates. Here, we show that the midgut-derived hormone, Neuropeptide F (NPF), acts as the sugar-responsive, an incretin-like hormone in the fruit fly, Drosophila melanogaster. Secreted NPF is received by NPF receptor in the corpora cardiaca and in insulin-producing cells. NPF-NPFR signalling resulted in the suppression of the glucagon-like hormone production and the enhancement of the insulin-like peptide secretion, eventually promoting lipid anabolism. Similar to the loss of incretin function in mammals, loss of midgut NPF led to significant metabolic dysfunction, accompanied by lipodystrophy, hyperphagia, and hypoglycaemia. These results suggest that enteroendocrine hormones regulate sugar-dependent metabolism through glucagon-like and insulin-like hormones not only in mammals but also in insects.

show abstract

Modulation of metabolic hormone signalingviaa circadian hormone and a biogenic amine inDrosophila melanogaster

Cited by 7 publications

References 60 publications

The Intrinsic Nutrient Sensing Adipokinetic Hormone Producing Cells Function in Modulation of Metabolism, Activity, and Stress

The Intrinsic Nutrient Sensing Adipokinetic Hormone Producing Cells Function in Modulation of Metabolism, Activity, and Stress

Endocrine fine-tuning of daily locomotor activity patterns under non-starving conditions in Drosophila

The sugar-responsive enteroendocrine neuropeptide F regulates lipid metabolism through glucagon-like and insulin-like hormones inDrosophila melanogaster

Contact Info

Product

Resources

About