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Excess glucose or fat differentially affects metabolism and appetite-related gene expression during zebrafish embryogenesis.

ABSTRACT: Zebrafish embryos use their yolk sac reserve as the sole nutrient source during embryogenesis. The two main forms of energy fuel can be found in the form of glucose or fat. Zebrafish embryos were exposed to glucose or injected with free fatty acid/Triacylglycerol (FFA/TAG) into the yolk sac at 24 hpf. At 72 hpf, glucose exposed or FFA/TAG injected had differential effects on gene expression in embryos, with fat activating lipolysis and β-oxidation and glucose activating the insulin pathway. Bulk RNA-seq revealed that more gene expression was affected by glucose exposure compared to FFA/TAGs injection. Appetite-controlling genes were also differently affected by glucose exposure or FFA/TAG injections. Because the embryo did not yet feed itself at the time of our analysis, gene expression changes occurred in absence of actual hunger and revealed how the embryo manages its nutrient intake before active feeding.

SUBMITTER: Konadu B

PROVIDER: S-EPMC10391732 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Excess glucose or fat differentially affects metabolism and appetite-related gene expression during zebrafish embryogenesis.

Konadu Bridget B Cox Carol K CK Garrett Michael R MR Gibert Yann Y

iScience 20230607 7

Zebrafish embryos use their yolk sac reserve as the sole nutrient source during embryogenesis. The two main forms of energy fuel can be found in the form of glucose or fat. Zebrafish embryos were exposed to glucose or injected with free fatty acid/Triacylglycerol (FFA/TAG) into the yolk sac at 24 hpf. At 72 hpf, glucose exposed or FFA/TAG injected had differential effects on gene expression in embryos, with fat activating lipolysis and β-oxidation and glucose activating the insulin pathway. Bulk ...[more]

PMID: 37534154

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Project description:Background: Appetite disorders are frequent and scantly studied in peritoneal dialysis (PD) patients and are associated with malnutrition and cardiovascular complications. Objective: We investigated the relationship between uremic insulin resistance, pro-inflammatory cytokines, and appetite-related peptides release (ARPr) with eating-behavior disorders in PD patients. Methods: We included 42 PD patients (12 suffering anorexia, 12 obese with high food-intake, and 18 asymptomatic) and 10 controls. We measured blood levels of ARPr including orexigens [neuropeptide-Y (NPY), ghrelin, and nitric-oxide], anorexigens [cholecystokinin, insulin, corticotropin-releasing factor, leptin, and adiponectin (Ad)], and cytokines (TNF-α, sTNFα-R2, and IL-6) both at baseline and after administering a standard-food stimulus (SFS). We also measured the expression of TNF-α, leptin and Ad-encoding mRNAs in abdominal adipose tissue. We compared these markers with eating motivation measured by a Visual Analog Scale (VAS). Results: Anorexics showed both little appetite, measured by a VAS, and low levels of orexigens that remained constant after SFS, coupled with high levels of anorexigens at baseline and after SFS. Obeses showed higher appetite, increased baseline levels of orexigens, lower baseline levels of anorexigens and cytokines and two peaks of NPY after SFS. The different patterns of ARPr and cytokines pointed to a close relationship with uremic insulin resistance. In fact, the euglycemic-hyperglycemic clamp reproduced these disorders. In anorexics, TNF-α fat expression was increased. In obese patients, leptin expression in fat tissue was down-regulated and showed correlation with the appetite. Conclusion: In PD, appetite is governed by substances that are altered at baseline and abnormally released. Such modulators are controlled by insulin metabolism and cytokines and, while anorexics display inflammatory predominance, obese patients predominantly display insulin resistance.

Project description:BACKGROUND: The mosquito A. aegypti is vector of dengue and other viruses. New methods of vector control are needed and can be achieved by a better understanding of the life cycle of this insect. Embryogenesis is a part of A. aegypty life cycle that is poorly understood. In insects in general and in mosquitoes in particular energetic metabolism is well studied during oogenesis, when the oocyte exhibits fast growth, accumulating carbohydrates, lipids and proteins that will meet the regulatory and metabolic needs of the developing embryo. On the other hand, events related with energetic metabolism during A. aegypti embryogenesis are unknown. RESULTS: Glucose metabolism was investigated throughout Aedes aegypti (Diptera) embryonic development. Both cellular blastoderm formation (CBf, 5 h after egg laying - HAE) and germ band retraction (GBr, 24 HAE) may be considered landmarks regarding glucose 6-phosphate (G6P) destination. We observed high levels of glucose 6-phosphate dehydrogenase (G6PDH) activity at the very beginning of embryogenesis, which nevertheless decreased up to 5 HAE. This activity is correlated with the need for nucleotide precursors generated by the pentose phosphate pathway (PPP), of which G6PDH is the key enzyme. We suggest the synchronism of egg metabolism with carbohydrate distribution based on the decreasing levels of phosphoenolpyruvate carboxykinase (PEPCK) activity and on the elevation observed in protein content up to 24 HAE. Concomitantly, increasing levels of hexokinase (HK) and pyruvate kinase (PK) activity were observed, and PEPCK reached a peak around 48 HAE. Glycogen synthase kinase (GSK3) activity was also monitored and shown to be inversely correlated with glycogen distribution during embryogenesis. CONCLUSIONS: The results herein support the hypothesis that glucose metabolic fate changes according to developmental embryonic stages. Germ band retraction is a moment that was characterized as a landmark in glucose metabolism during Aedes aegypti embryogenesis. Furthermore, the results also suggest a role for GSK3 in glycogen balance/distribution during morphological modifications.

Dataset Information

Excess glucose or fat differentially affects metabolism and appetite-related gene expression during zebrafish embryogenesis.

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Excess glucose or fat differentially affects metabolism and appetite-related gene expression during zebrafish embryogenesis.

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