ABSTRACT: Mosquitos were fed sugar water or blood. The blood fed mosquitos were given 6 h or 24 h to digest. The midguts were dissected and prepared for MSP-MS.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. To gain insight into the mechanisms underlying this response, we profiled gene expression in chronically high sugar fed, wandering (post-prandial) third instar wild type larvae (L3). These data were compared to control-fed larvae as well as those (mid-L3) actively feeding for twelve hours on both diets. We used microarrays to detail the response of Drosophila larvae to high sugar-induced insulin resistance.
Project description:Chronic high-sugar feeding (1 M or 34% sucrose) leads to hyperglycemia, obesity, and insulin resistance in adult flies, compared with those fed a control diet (0.15 M or 5% sucrose). We compared two days and four weeks of high-sugar feeding to look at short- and long- term effects on gene expression. We used Affymetrix Drosophila GeneChip 2.0 microarrays to quantify differential expression between control and high-sugar-fed flies at two time points.
Project description:High sugar consumption, as well as high-fat diet, is a known cause of obesity and metabolic syndrome. However, the synergistic effect of high-sugar and high-fat consumption rarely has been evaluated, especially in terms of transcriptional regulation. Therefore, we focused on the effect of high sugar consumption on hepatic transcriptional networks in normal and high fat-fed mice. C57BL/6J mice were divided into four groups and were provided either 23%(w/v) sugar solution or plain water with either high-fat or normal-fat diet for 10 weeks. As a result, high sugar consumption significantly altered lipid metabolism-related genes in normal fat-fed mice; however, in high fat-fed mice, high sugar consumption altered inflammation-responsive genes rather than lipid metabolism. After all, these modulations eventually increased lipid accumulation in the liver and caused systemic metabolic disturbances. These observations for the first time suggested that high sugar consumption along with high-fat diet could lead to the development of severe metabolic syndrome via altering hepatic transcriptional networks.
Project description:Chronic high sugar feeding induces obesity, hyperglycemia, and insulin resistance in flies and mammals. To gain insight into the mechanisms underlying this response, we profiled gene expression in chronically high sugar fed, wandering (post-prandial) third instar wild type larvae (L3). These data were compared to control-fed larvae as well as those (mid-L3) actively feeding for twelve hours on both diets. We used microarrays to detail the response of Drosophila larvae to high sugar-induced insulin resistance. Male Canton-S third instar larvae were fed control (0.15M) or high (1M) sucrose and selected for RNA extraction and hybridization on Affymetrix microarrays. Wandering L3 were selected as those in the top half of the vial with partial blue guts to confirm that they had stopped eating the (blue) food. Mid-L3 were selected as L2, aged overnight until early L3, then transferred to fresh control or high sucrose food for 12 more hours before selection.
Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed among the experimental mice fed four different dietary components. Methods: We carried out RNA-Seq analysis of ileum tissue from 6 weeks male mice ad libitum fed for 10 weeks a high liquid sugar (23% (w/v)) or/and high fat (60% Kcal from fat) diet. The combined effect of sugar drink and high fat diet (HF-Sugar) was compared with sugar drink only (NF-Sugar), or high fat diet only (HF), or control diet that was plain water and normal fat diet (NF). Results: RNA-Seq revealed sample-specific clusters that included genes responding to each experimental diet. We found only addition of sugar drink to high fat group (HF-Sugar) not NF-Sugar and HF, there was a significant enrichment in biological functions relating to Inflammatory/Immune Responses, especially including dendritic cell (DC) and T cell related signaling pathway. Conclusions: Taken together, our data demonstrate that sugar drink synergistically promotes and exacerbates inflammatory responses driven by the high fat diet.
Project description:Conditionally pathogenic gut microbes promote larval growth by increasing redox-dependent fat storage in high sugar diet-fed Drosophila melanogaster
Project description:We report here RNAseq analysis of the comparison of gene expression between sugar fed and blood fed Aedes aegypti ovaries, to understand blood meal induced changes in gene expression.
Project description:The effect of chloroquine on mosquitoes transcript abundance was assayed by comparing gene expression between mosquitoes fed on a blood meal containing 50 mg/Kg of chloroquine and those that had fed on a normal blood meal. Pools of 50 midguts were dissected and were hybridize with MMC1 (or 20K) microarrays. <br><br>Anopheles gambiae female mosquitoes were blood fed on BALB/c mice infected with P. berghei and intraperitonally pre-treated with 50 mg/kg of chloroquine. As controls, mosquitoes were blood fed on untreated P. berghei infected mice.<br><br>Mosquitoes were collected 24 hours post-blood feeding and pools of 50 midguts were dissected and processed for hybridization with MMC1 (or 20K) microarrays.Two different biological experiments were performed for each treatment.