Parental dietary protein-to-carbohydrate ratio affects offspring lifespan and metabolism in drosophila

Strilbytska, Olha; Velianyk, Vira; Burdyliuk, Nadia; Yurkevych, Ihor S.; Vaiserman, Alexander; Storey, Kenneth B.; Pospisilik, Andrew; Lushchak, Oleh

doi:10.1016/j.cbpa.2019.110622

Cited by 21 publications

(42 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this sense, not only the caloric overload plays a role, but also the type of substrate (type of sugar, for example) 33 , 59 and the relationship between macronutrients (protein–sugar–fat ratio) 60 . Additionally, the effects of diet can exert transgenerational changes, modulating the size, reproductive capacity and survival of the offspring 61 . The effects of a diet rich in calories, particularly rich in sugar, are metabolically manifested in energy storage 33 , 59 .…”

Section: Discussionmentioning

confidence: 99%

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster

Lourido

Quenti

Salgado-Canales

et al. 2021

Sci Rep

View full text Add to dashboard Cite

Insulin resistance is a hallmark of type 2 diabetes resulting from the confluence of several factors, including genetic susceptibility, inflammation, and diet. Under this pathophysiological condition, the dysfunction of the adipose tissue triggered by the excess caloric supply promotes the loss of sensitivity to insulin at the local and peripheral level, a process in which different signaling pathways are involved that are part of the metabolic response to the diet. Besides, the dysregulation of insulin signaling is strongly associated with inflammatory processes in which the JAK/STAT pathway plays a central role. To better understand the role of JAK/STAT signaling in the development of insulin resistance, we used a simple organism, Drosophila melanogaster, as a type 2 diabetes model generated by the consumption of a high-sugar diet. In this model, we studied the effects of inhibiting the expression of the JAK/STAT pathway receptor Domeless, in fat body, on adipose metabolism and glycemic control. Our results show that the Domeless receptor loss in fat body cells reverses both hyperglycemia and the increase in the expression of the insulin resistance marker Nlaz, observed in larvae fed a high sugar diet. This effect is consistent with a significant reduction in Dilp2 mRNA expression and an increase in body weight compared to wild-type flies fed high sugar diets. Additionally, the loss of Domeless reduced the accumulation of triglycerides in the fat body cells of larvae fed HSD and also significantly increased the lifespan of adult flies. Taken together, our results show that the loss of Domeless in the fat body reverses at least in part the dysmetabolism induced by a high sugar diet in a Drosophila type 2 diabetes model.

show abstract

Section: Discussionmentioning

confidence: 99%

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster

Lourido

Quenti

Salgado-Canales

et al. 2021

Sci Rep

View full text Add to dashboard Cite

show abstract

“…The dietary formulations, and use of the Alstonville strain were the same, but there were key differences such as the number of generations that were exposed to a particular diet, and the number of fly strains used. It was essential to change the study design to remove the influence of parental diet on offspring development which have been well described (Emborski and Mikheyev, 2019;Guida et al, 2019;Matzkin et al, 2013;Strilbytska et al, 2020;Valtonen et al, 2012;Vijendravarma et al, 2010;Zajitschek et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…Ancestral environmental changes that have been found to alter phenotypes of descendants include behavioural stress, toxin exposure and nutritional variation (Cavalli and Heard, 2019;Legoff et al, 2019;Perez and Lehner, 2019). The latter is perhaps the most-studied, and examples of ancestral diet altering descendent phenotype have been documented due to overor under-nutrition in natural populations including human (Aiken and Ozanne, 2014) and laboratory organisms such as Caenorhabditis elegans (Kishimoto et al, 2017;Tauffenberger and Parker, 2014), Drosophila (Emborski and Mikheyev, 2019;Ost et al, 2014;Strilbytska et al, 2020;Vijendravarma et al, 2010;Xia et al, 2016) and rodents (Aiken and Ozanne, 2014). In these studies changes to descendent metabolism and growth is often reported, resulting in developmental timing, organ size and body weight alterations.…”

Section: Introductionmentioning

confidence: 99%

“…We hypothesised that the generational differences could be due to transgenerational epigenetic inheritance effects that altered the rate at which the flies progress through the developmental stages of embryo, larva, pupae, and adult. Importantly, these effects appeared to be somewhat accumulated across generations suggesting that they were not solely caused by the diet that the fly was consuming when it produced its gametes (Strilbytska et al, 2020;Vijendravarma et al, 2010). We therefore designed our experiments to exclude parental effects by ensuring that all parents consumed the same diet, and variation in ancestral diet was limited to the grand-parental and great grand-parental generations (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ancestral dietary change alters development ofDrosophilalarvae through MAPK signalling

Towarnicki

Youngson

Corley

et al. 2020

Preprint

View full text Add to dashboard Cite

Increasing evidence in animal species ranging from mammals to insects has revealed phenotypes that are caused by ancestral life experiences including stress and diet. The descendent phenotypes themselves are wide ranging, and include changes to behaviour, disease risk, metabolism, and growth. Ancestral dietary macronutrient composition, and quantity (over- and under-nutrition) have been shown to alter descendent growth, metabolism and behaviour. Several studies have identified inherited molecules in gametes which are altered by ancestral diet and are required for the transgenerational effect. However, there is less understanding of the developmental pathways in the period between fertilisation and adulthood that are altered by the inherited molecules. Here we identify a key role of the MAPK signalling pathway in mediating changes to Drosophila larval developmental timing due to variation in ancestral diet. We exposed grand-parental and great grand-parental generations to defined protein to carbohydrate (P:C) dietary ratios and measured developmental timing. Descendent developmental timing was consistently faster in the period between the embryonic and pupal stages when the ancestor had a higher P:C ratio diet. Transcriptional analysis of embryos, larvae and adults revealed extensive and long-lasting changes to the MAPK signalling pathway which controlled growth rate through regulation of ribosomal RNA transcription. The importance of these processes was supported by pharmacological inhibition of MAPK and rRNA proteins which reproduced the ancestral diet-induced developmental changes. This work provides insight into the role of developmental growth signalling networks in mediating non-genetic inheritance in the period between fertilisation and adult.Summary statementAncestral, diet-induced descendent developmental timing changes are caused by alteration of MAPK signalling pathways in the period between the embryo and pupal stages in Drosophila.

show abstract

“…Genetic prerequisites, disrupted sleep, chronic emotional stress and other stresses like xenobiotic exposure, unbalanced food, alterations in gut microbiota composition, and getting older are among other important risk factors involved in MetS development and progression and are deeply described elsewhere [2,6,9,12,30,[35][36][37]. In addition, a number of studies suggest that parental obesity can lead to fetal metabolic reprogramming and to development of obesity and metabolic dysfunction in the offspring [33,34,38,39]. Newborns from obese fathers had altered DNA methylation overall and significant hypomethylation at the insulin-like growth factor 2 (IGF2) gene.…”

Section: Epidemiology Causes and Complications Of Metsmentioning

confidence: 99%

Metabolic Syndrome, Obesity, and Drosophila

Bayliak

2020

jpnu

View full text Add to dashboard Cite

Metabolic syndrome (MetS) is a cluster of metabolic disturbances increasing a risk of cardiovascular diseases and diabetes 2 types. The main features of MetS include atherogenic dyslipidemia, elevated blood pressure, insulin resistance and elevated glucose levels, a pro-thrombotic state, pro-oxidant and pro-inflammatory states. Excessive consumption of high caloric food and sedentary lifestyle followed by overweight and obesity, as well as aging and stresses are major contributing factors to the MetS development. MeS affects between 10 and 84% of adults depending on the used MetS criteria and increases significantly a risk of cardiovascular diseases, diabetes 2 type and kidney diseases. Patients with metabolic disorders like obesity, diabetes, cardiovascular, and liver disease may have a higher risk of infection of COVID-19 with significantly worse prognosis and outcomes in these patients. In recent years, the fruit fly, Drosophila melanogaster, has been actively used to study human metabolic disorders as a cost-effective and expedient model. Drosophila belongs to insects with full metamorphosis and its life cycle includes four developmental stages: embryo, larva, pupa, and adult flies. Each developmental stage has its own specific advantages and can be used to study metabolic homeostasis. Studies of metabolic disturbances in Drosophila and mammalian models along with humans have demonstrated that flies and small mammalian models have many similarities with humans in basic metabolic functions and share many molecular mechanisms which regulate these metabolic processes. In this paper, we describe the advantages and limitations of Drosophila models of metabolic syndrome and obesity in light of physiological and biochemical similarities and differences between insects and mammals.

show abstract

Parental dietary protein-to-carbohydrate ratio affects offspring lifespan and metabolism in drosophila

Cited by 21 publications

References 49 publications

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster

Domeless receptor loss in fat body tissue reverts insulin resistance induced by a high-sugar diet in Drosophila melanogaster

Ancestral dietary change alters development ofDrosophilalarvae through MAPK signalling

Metabolic Syndrome, Obesity, and Drosophila

Contact Info

Product

Resources

About