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Paternal zinc deficiency alters offspring metabolic status in Drosophila melanogaster
被引:0
|作者:
Sanusi, Kamaldeen Olalekan
[1
,2
,3
]
Ibrahim, Kasimu Ghandi
[1
,2
,4
,5
]
Abubakar, Murtala Bello
[6
]
Imam, Mustapha Umar
[1
,7
]
机构:
[1] Usmanu Danfodiyo Univ, Ctr Adv Med Res & Training, Sokoto, Nigeria
[2] Usmanu Danfodiyo Univ, Coll Hlth Sci, Fac Basic Med Sci, Dept Physiol, Sokoto, Nigeria
[3] Al Hikmah Univ, Fac Hlth Sci, Dept Human Physiol, PMB 1601, Ilorin, Nigeria
[4] Zarqa Univ, Fac Dent, Dept Basic Med & Dent Sci, POB 2000, Zarqa 13110, Jordan
[5] Univ Witwatersrand, Fac Hlth Sci, Sch Physiol, 7 York Rd, ZA-2193 Johannesburg, South Africa
[6] Sultan Qaboos Univ, Coll Med & Hlth Sci, Dept Physiol, Muscat, Oman
[7] Usmanu Danfodiyo Univ Sokoto, Coll Hlth Sci, Fac Basic Med Sci, Dept Med Biochem, Sokoto, Nigeria
关键词:
Zinc deficiency;
Drosophila melanogaster;
Intergenerational effects;
Paternal influence;
Metabolic alterations;
INFLAMMATION;
PLASMA;
D O I:
10.1016/j.jtemb.2024.127519
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Background: This study delves into the understudied yet potentially crucial role of paternal zinc deficiency in programming offspring metabolic outcomes. By examining paternal zinc deficiency, we aim to shed light on a previously unexplored avenue with the potential to significantly impact future generations. We investigated the intergenerational effects of paternal zinc deficiency on metabolic parameters in Drosophila melanogaster. Methods: Dietary zinc deficiency was induced by supplementing the diet of Drosophila F0 male flies with TPEN (N,N,N ',N '-tetrakis(2-pyridylmethyl)ethylenediamine) from egg stage. The F0 male flies after eclosion were mated with age-matched virgin female flies from the control group, resulting in the F1 offspring generation. The F1 generation were then cultured on a standard diet for subsequent metabolic analyses, including assessments of body weight, locomotion, and levels of glucose, trehalose, glycogen, and triglycerides as well as the expression of related genes. Results: We observed an increase (p<0.05) in body weight in male parent flies and female offspring. Negative geotaxis performance was also impaired in the female offspring. Paternal zinc deficiency exerted distinct effects on carbohydrate and lipid metabolism, as evidenced by a significant (p<0.05) increase in trehalose and triglyceride levels in both parent and offspring. Additionally, zinc deficiency led to alterations in the expression of key metabolic genes, including significant (p<0.05) increase in DILP2 mRNA levels, highlighting potential links to insulin signaling. Also, there were reduced mRNA levels of SOD1 and CAT in both parental and offspring generations. Parental zinc deficiency also increased the expression of Eiger and UPD2 mRNA in the offspring, suggesting potential perturbations in the immune response system. Conclusion: These findings underscore the link between zinc status and various physiological and molecular processes, revealing both immediate and intergenerational impacts on metabolic, antioxidant, and inflammatory pathways and providing valuable insights on the implications of paternal zinc deficiency in Drosophila melanogaster.
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