Drosophila dFOXO controls lifespan and regulates insulin signalling in brain and fat body

Nature ◽  
2004 ◽  
Vol 429 (6991) ◽  
pp. 562-566 ◽  
Author(s):  
Dae Sung Hwangbo ◽  
Boris Gersham ◽  
Meng-Ping Tu ◽  
Michael Palmer ◽  
Marc Tatar
Keyword(s):  
Fat Body ◽  
Insulin Signalling

scholarly journals Erratum: Drosophila dFOXO controls lifespan and regulates insulin signalling in brain and fat body

Nature ◽  
2005 ◽  
Vol 434 (7029) ◽  
pp. 118-118 ◽  
Author(s):  
Dae Sung Hwangbo ◽  
Boris Gershman ◽  
Meng-Ping Tu ◽  
Michael Palmer ◽  
Marc Tatar
Keyword(s):  
Fat Body ◽  
Insulin Signalling

scholarly journals Edem1 activity in the fat body regulates insulin signalling and metabolic homeostasis in Drosophila

2019 ◽  
Author(s):  
Himani Pathak ◽  
Jishy Varghese
Keyword(s):  
Protein Quality ◽  
Fat Body ◽  
Insulin Signalling ◽  
Nutrient Status ◽  
Vital Role ◽  
Metabolic Homeostasis ◽  
Humoral Factors ◽  
Mammalian Liver ◽  
Nutrient Environment ◽  
Pleiotropic Functions

AbstractIn Drosophila, nutrient status is sensed by the fat body, a functional homolog of mammalian liver and white adipocytes. The fat body conveys nutrient information to insulin-producing cells (IPCs) through humoral factors which regulate Drosophila insulin-like peptide (DILP) levels and insulin signalling. Insulin signalling has pleiotropic functions, which include the management of growth and metabolic pathways. Here, we report that Edem1 (endoplasmic reticulum degradation-enhancing α-mannosidase-like protein 1), an endoplasmic reticulum-resident protein involved in protein quality control, acts in the fat body to regulate insulin signalling and thereby the metabolic status in Drosophila. Edem1 limits the fat body derived Drosophila TNFα Eiger activity on IPCs and maintains systemic insulin signalling in fed conditions. During food deprivation, edem1 gene expression levels drop, which aids in the reduction of systemic insulin signalling crucial for survival. Overall we demonstrate that Edem1 plays a vital role in helping the organism to endure a fluctuating nutrient environment by managing insulin signalling and metabolic homeostasis.

scholarly journals Tissue-specific modulation of gene expression in response to lowered insulin signalling in Drosophila

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Luke Stephen Tain ◽  
Robert Sehlke ◽  
Ralf Leslie Meilenbrock ◽  
Thomas Leech ◽  
Jonathan Paulitz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Fat Body ◽  
Insulin Signalling ◽  
Health Improvement ◽  
Proteomic Profiling ◽  
Protein Subunit ◽  
Altered Expression ◽  
Tissue Specific ◽  
Age Related ◽  
Specific Regulation

Reduced activity of the insulin/IGF signalling network increases health during ageing in multiple species. Diverse and tissue-specific mechanisms drive the health improvement. Here, we performed tissue-specific transcriptional and proteomic profiling of long-lived Drosophila dilp2-3,5 mutants, and identified tissue-specific regulation of >3600 transcripts and >3700 proteins. Most expression changes were regulated post-transcriptionally in the fat body, and only in mutants infected with the endosymbiotic bacteria, Wolbachia pipientis, which increases their lifespan. Bioinformatic analysis identified reduced co-translational ER targeting of secreted and membrane-associated proteins and increased DNA damage/repair response proteins. Accordingly, age-related DNA damage and genome instability were lower in fat body of the mutant, and overexpression of a minichromosome maintenance protein subunit extended lifespan. Proteins involved in carbohydrate metabolism showed altered expression in the mutant intestine, and gut-specific overexpression of a lysosomal mannosidase increased autophagy, gut homeostasis, and lifespan. These processes are candidates for combatting ageing-related decline in other organisms.

scholarly journals Insulin signalling regulates remating in female Drosophila

2010 ◽  
Vol 278 (1704) ◽  
pp. 424-431 ◽  
Author(s):  
Stuart Wigby ◽  
Cathy Slack ◽  
Sebastian Grönke ◽  
Pedro Martinez ◽  
Federico C. F. Calboli ◽  
...  
Keyword(s):  
Fat Body ◽  
Insulin Signalling ◽  
Underlying Mechanism ◽  
Neurosecretory Cells ◽  
Dominant Negative ◽  
Developmental Defects ◽  
Mating Rate ◽  
Female Remating ◽  
Reduced Body ◽  
Median Neurosecretory Cells

Mating rate is a major determinant of female lifespan and fitness, and is predicted to optimize at an intermediate level, beyond which superfluous matings are costly. In female Drosophila melanogaster , nutrition is a key regulator of mating rate but the underlying mechanism is unknown. The evolutionarily conserved insulin/insulin-like growth factor-like signalling (IIS) pathway is responsive to nutrition, and regulates development, metabolism, stress resistance, fecundity and lifespan. Here we show that inhibition of IIS, by ablation of Drosophila insulin-like peptide (DILP)-producing median neurosecretory cells, knockout of dilp2 , dilp3 or dilp5 genes, expression of a dominant-negative DILP-receptor ( InR ) transgene or knockout of Lnk , results in reduced female remating rates. IIS-mediated regulation of female remating can occur independent of virgin receptivity, developmental defects, reduced body size or fecundity, and the receipt of the female receptivity-inhibiting male sex peptide. Our results provide a likely mechanism by which females match remating rates to the perceived nutritional environment. The findings suggest that longevity-mediating genes could often have pleiotropic effects on remating rate. However, overexpression of the IIS-regulated transcription factor dFOXO in the fat body—which extends lifespan—does not affect remating rate. Thus, long life and reduced remating are not obligatorily coupled.

scholarly journals Edem1 activity in the fat body regulates insulin signalling and metabolic homeostasis in Drosophila

2021 ◽  
Vol 4 (8) ◽  
pp. e202101079
Author(s):  
Himani Pathak ◽  
Jishy Varghese
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Quality ◽  
Fat Body ◽  
Insulin Signalling ◽  
Nutrient Status ◽  
Vital Role ◽  
Metabolic Homeostasis ◽  
Humoral Factors ◽  
Insulin Producing Cells ◽  
Factor Α

In Drosophila, nutrient status is sensed by the fat body, a functional homolog of mammalian liver and white adipocytes. The fat body conveys nutrient information to insulin-producing cells through humoral factors which regulate Drosophila insulin-like peptide levels and insulin signalling. Insulin signalling has pleiotropic functions, which include the management of growth and metabolic pathways. Here, we report that Edem1 (endoplasmic reticulum degradation–enhancing α-mannosidase–like protein 1), an endoplasmic reticulum–resident protein involved in protein quality control, acts in the fat body to regulate insulin signalling and thereby the metabolic status in Drosophila. Edem1 limits the fat body–derived Drosophila tumor necrosis factor-α Eiger activity on insulin-producing cells and maintains systemic insulin signalling in fed conditions. During food deprivation, edem1 gene expression levels drop, which aids in the reduction of systemic insulin signalling crucial for survival. Overall, we demonstrate that Edem1 plays a vital role in helping the organism to endure a fluctuating nutrient environment by managing insulin signalling and metabolic homeostasis.

scholarly journals Growth control through regulation of insulin-signaling by nutrition-activated steroid hormone

2017 ◽  
Author(s):  
Kurt Buhler ◽  
Jason Clements ◽  
Mattias Winant ◽  
Veerle Vulsteke ◽  
Patrick Callaerts
Keyword(s):  
Insulin Signaling ◽  
Growth Regulation ◽  
Fat Body ◽  
Insulin Signalling ◽  
Steroid Hormone ◽  
Growth Control ◽  
Important Variable ◽  
Growth Defects ◽  
Insulin Producing Cells ◽  
Growth Promoting

AbstractGrowth and maturation are coordinated processes in all animals. Integration of internal cues, such as signalling pathways, with external cues such as nutritional status is paramount for an orderly progression of development in function of growth. In Drosophila, this coordination involves insulin and steroid signalling, but the mechanisms by which this occurs and how they are coordinated are incompletely understood. We show that production of the bioactive 20-hydroxyecdysone by the enzyme Shade in the fat body is a nutrient-dependent process. We demonstrate that during fed conditions, Shade plays a role in growth regulation, as knockdown of shade in the fat body resulted in growth defects and perturbed expression and release of the Drosophila insulin-like peptides from the insulin-producing cells (IPCs). We identify the trachea and IPCs as direct targets through which 20-hydroxyecdysone regulates insulin-signaling. The identification of the trachea-dependent regulation of insulin-signaling exposes an important variable that may have been overlooked in other studies focusing on insulin-signaling in Drosophila. Finally, we show with IPC-specific manipulations that 20E may both be a growth-promoting and growth-inhibiting signal in the IPCs acting through different nuclear receptors. Our findings provide a potentially conserved, novel mechanism by which nutrition can modulate steroid hormone bioactivation, reveal an important caveat of a commonly used transgenic tool to study IPC function and yield further insights as to how steroid and insulin signalling are coordinated during development to regulate growth and developmental timing.

The Structure and Development of Microbodies in the Fat Body and other Tissues of an Insect (Calpodes Ethlius)

1970 ◽  
Vol 28 ◽  
pp. 148-149
Author(s):  
M. Locke ◽  
J. T. McMahon
Keyword(s):  
Electron Microscopy ◽  
Liquid Crystals ◽  
Fat Body ◽  
Competitive Inhibitor ◽  
Dense Core ◽  
Urate Oxidase ◽  
Blood Proteins ◽  
Free Base ◽  
The Core ◽  
The Matrix

The fat body of insects has always been compared functionally to the liver of vertebrates. Both synthesize and store glycogen and lipid and are concerned with the formation of blood proteins. The comparison becomes even more apt with the discovery of microbodies and the localization of urate oxidase and catalase in insect fat body.The microbodies are oval to spherical bodies about 1μ across with a depression and dense core on one side. The core is made of coiled tubules together with dense material close to the depressed membrane. The tubules may appear loose or densely packed but always intertwined like liquid crystals, never straight as in solid crystals (Fig. 1). When fat body is reacted with diaminobenzidine free base and H2O2 at pH 9.0 to determine the distribution of catalase, electron microscopy shows the enzyme in the matrix of the microbodies (Fig. 2). The reaction is abolished by 3-amino-1, 2, 4-triazole, a competitive inhibitor of catalase. The fat body is the only tissue which consistantly reacts positively for urate oxidase. The reaction product is sharply localized in granules of about the same size and distribution as the microbodies. The reaction is inhibited by 2, 6, 8-trichloropurine, a competitive inhibitor of urate oxidase.

L-Ascorbic Acid Addition to Chitosan Reduces Body Weight in Overweight Women

2014 ◽  
Vol 84 (1-2) ◽  
pp. 5-11 ◽  
Author(s):  
Eun Y. Jung ◽  
Sung C. Jun ◽  
Un J. Chang ◽  
Hyung J. Suh
Keyword(s):  
Ascorbic Acid ◽  
Body Weight ◽  
Fat Body ◽  
Body Weight Gain ◽  
Skinfold Thickness ◽  
The Body ◽  
Control Group ◽  
Percentage Body Fat ◽  
Overweight Women ◽  
Body Weights

Previously, we have found that the addition of L-ascorbic acid to chitosan enhanced the reduction in body weight gain in guinea pigs fed a high-fat diet. We hypothesized that the addition of L-ascorbic acid to chitosan would accelerate the reduction of body weight in humans, similar to the animal model. Overweight subjects administered chitosan with or without L-ascorbic acid for 8 weeks, were assigned to three groups: Control group (N = 26, placebo, vehicle only), Chito group (N = 27, 3 g/day chitosan), and Chito-vita group (N = 27, 3 g/day chitosan plus 2 g/day L-ascorbic acid). The body weights and body mass index (BMI) of the Chito and Chito-vita groups decreased significantly (p < 0.05) compared to the Control group. The BMI of the Chito-vita group decreased significantly compared to the Chito group (Chito: -1.0 kg/m2 vs. Chito-vita: -1.6 kg/m2, p < 0.05). The results showed that the chitosan enhanced reduction of body weight and BMI was accentuated by the addition of L-ascorbic acid. The fat mass, percentage body fat, body circumference, and skinfold thickness in the Chito and Chito-vita groups decreased more than the Control group; however, these parameters were not significantly different between the three groups. Chitosan combined with L-ascorbic acid may be useful for controlling body weight.

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