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Poster Full Abstracts - Drosophila Models of Human Diseases
Poster board number is above title. The first author is the presenter
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rapid platform to test the effects of genes or drugs. We developed a Drosophila model of T2D (mT2D) by feeding developing larvae a high sugar diet (HSD,
1M sucrose, Musselman et al 2011). Tissue-specific loss-of-function studies reveal that the fat body plays an important role in controlling the whole animal
response to dietary excess. Fat accumulation is a protective mechanism in the face of a HSD, because genetic manipulations that decrease the capacity of
flies to store triglycerides result in enhanced diabetic phenotypes. Flux of dietary carbon into storage as fat is abrogated in larvae reared on the HSD despite
an increase in expression of genes encoding glycolysis and lipogenesis enzymes. We present evidence for novel susceptibility genes and those that protect
against diet-induced diabetes in Drosophila. These studies should provide insights into mechanisms of insulin resistance and should identify potential
therapeutic targets.
403A
Lipid and carbohydrate analysis on a Drosophila melanogaster Type 2 Diabetes model.
Alejandro Reyes De la Torre, Juan Riesgo-Escovar.
Developmental neurobiology and neurophysiology, Instituto de Neurobiologia, UNAM, Queretaro, Mexico.
Type 2 diabetes is a chronic disease characterized by peripheral insulin resistance, high glucose, and elevated free fatty acids. Insulin is an anabolic
hormone whose signaling pathway is highly conserved from nematodes to vertebrates. In Drosophila melanogaster insulin pathway mutants, larvae and 1-2
day old adults have elevated lipid and carbohydrate levels, yet chronic aspects of these type 2 diabetes models have not been investigated. In this work, we
measured total lipid and carbohydrate levels from wild type and homozygous mutant chico1/chico1 adult female flies at 1, 7, 14 and 28 days. chico is the fly
insulin receptor substrate homologue. Also, we studied lipid droplets in isolated abdominal adipocytes with Nile Red in homozygous chico1/chico1 flies, and
heteroallelic mutant Dp110A/Dp1105W3, InRE19/InR3T5, PKB1/PKB3 and S6KL-1/S6KP1713one day old adult flies and controls. DP110 is the catalytic
subunit of the fly PI3 kinase; InR is the fly insulin receptor, PKB is the fly protein kinase B, and S6K is the fly S6 kinase. Results show significant
differences in total lipids between wild type and chico1/chico1 flies at 1, 14 and 28 days (P<0.001). Moreover, there are significant differences in total
carbohydrates between wild type and chico1/chico1 flies at 14 days (P<0.001). We conclude that lipid and carbohydrate homeostasis is altered in chico
mutant flies, as there are no significant changes in lipids or carbohydrates throughout time in adult wild type flies. Preliminary results also show that there
are no significant differences in lipid volume in abdominal adipocytes between control and mutant flies. So, differences in total lipids may be given by total
abdominal adipocyte number instead of lipid accumulation in mutant abdominal adipocytes, or by accumulation of lipids in other tissues in mutants.
Acknowledgements: We thank Dr. Ma. Teresa Peña-Rangel for expert technical assistance, Ana Laura Pinedo Vargas and Claudia González Flores.
Funding: UNAM, CONACYT scholarship 369737.
404B
Identifying Genes Involved in Central Nervous System Control of Obesity.
Irene Trinh
1,2
, Oxana Gluscencova
1
, Gabrielle Boulianne
1,2
. 1) Hospital for
Sick Children, Toronto, Ontario, Canada; 2) University of Toronto, Toronto, Ontario, Canada.
The increasing prevalence of obesity as well as its association with many chronic diseases have turned obesity into a major health concern worldwide.
Obesity has many underlying environmental and genetic factors that both contribute to disturb the homeostatic mechanisms that maintain a balance between
energy intake and energy expenditure. At the top of the hierarchy is the central nervous system which regulates energy homeostasis by integrating inputs
from the periphery and producing the appropriate outputs to the metabolic organs. However, despite the amount of attention given to this neuronal circuitry,
the signalling pathways and underlying mechanisms are still not clearly defined. The goal of my project is to help further our understanding of these CNS
mechanisms by using the powerful tools available in Drosophila melanogaster to identify neuronal genes involved in energy homeostasis. Specifically, I
screened to see if knockdown of individual genes in the CNS would produce obese or lean phenotypes defined as increases or decreases in fat stores
respectively. To date, I have completed screening 1700 genes producing 107 hits that when knocked down in fru-Gal4-expressing neurons that results in
greater than 30 percent change in the levels of stored lipids compared to a fru-Gal4/wt control.
405C
The effect of three types of diets on the phenotype of Drosophila melanogaster.
Xiangpei Zeng, Sean Mendez, Laura Reed. Department of Biological
Sciences, University of Alabama, Tuscaloosa, AL.
The increasing frequency of Metabolic Syndrome in modern society suggests that changes in the human environment can predispose individuals to express
cryptic genetic variation for metabolic disease. This might be due either to alterations in diets or the interaction of diet with the underlying genetic variations
in the population. To contrast the effect of different types of food on phenotype, we have focused on the effect of three types of food on several metabolic
traits in several inbred lines of Drosophila melanogaster. Specifically, we are interested in contrasting the effect of added fat in a low sugar or a high sugar
diet. We used three types of food in this experiment: normal food (N), normal food with high fat (NF), and low sugar food with high fat (OF). Three
phenotypes were measured: pupae weight, total triglyceride content, and trehalose content. We found significant interactions between the genetic lines and
the diets for the phenotypes. Differences between metabolic traits mean and variance in response to three types of diets indicates that alterations in diets
could contribute to the changes in phenotype of four inbred lines of Drosophila melanogaster, with independent contributions of sugar and fat effects.
406A
Suppression of progressive motor neuron degeneration by Diferuloylmethane (Curcumin) in transgenic Drosophila expressing mutant human gene
of neurodegenerative disease.
Namita Agrawal, Anjalika Chongtham, Nidhi Paliwal. Dept of Zoology, University of Delhi, Delhi.
Huntington’s disease (HD) is a progressive neurodegenerative disorder caused by an expansion of a homopolymeric polyglutamine (polyQ) stretch within
the huntingtin protein (Htt) The fruit fly, Drosophila melanogaster has been proved a very powerful invertebrate model for testing drugs. Drosophila
transgenic model engineered to express mutant human genes of neurodegenerative disease like Huntington disease (HD) has been used previously by us to
test effectiveness of the drug combinations for the treatment of the HD pathogenesis (Agrawal et al., PNAS 2005). This model has been proven to be
excellent models of these largely dominant human diseases by replicating most of the disease symptoms, such as late onset, reduced longevity,
neurodegeneration, and impaired motor function. To find a safe, non toxic drug for the pharmacologic treatment of devastating neurodegenerative diseases is
a real challenge in modern medicine. To circumvent this problem, a safe and suitable approach was used by testing some popular phytochemicals which are
known for several thousand years in the world and are being used successfully for the treatment of various health conditions instead of pharmaceutical drugs.