You folks know me, so lets look at some science here
Below are just two studies I found pretty quickly. But both seem to indicate overfeeding is possible and likely detrimental.
Taddesse, F., Huh, M.D., Bai, S.C. and Vijverberg, J., 2014. Histological changes of liver in overfed young nile tilapia.
Journal of Fisheries and Aquatic Science,
9(2), pp.63-74.
Abstract :
We investigated histopathologically liver structural responses of Nile Tilapia
Oreochromis niloticus towards overfeeding. Mixed population of
O. niloticus with mean weight of 55±3.83 g was acclimated for one week. Then, the fish were separated into control and treatment groups. Glass aquariums with external biofilters and artificial heaters were used. Control and treatment groups were fed commercial Tilapia diet at 3 and 6% of fish body weight, respectively. Fish were dissected at three time intervals. Tissues were fixed, re-fixed, processed, embedded with paraffin and sectioned. Sectioned tissue ribbons were stained with hematoxylin and eosin technique for light microcopy. Hepatosomatic Index (HSI) and Hepatohypertrophic Index (HHI) were calculated. Irregular shaped hepatocytes with circular, conspicuous and centrally located nuclei were found from all control groups. Large hypertrophic hepatocytes with nuclei dislocated to the cell periphery observed after three weeks of overfeeding. Lipid vacuolation and atrophy were found after five weeks of overfeeding. Fish overfed for three weeks showed significantly (p<0.05) higher HSI and HHI values. Whereas, fish which were under third week control group showed the second significantly (p<0.05) higher HSI value. Significant (p<0.05) differences in HSI as well as HHI were not found between zero and fifth week control groups. We conclude that overfeeding may cause liver histological alterations in
O. niloticus and in turn lower aquaculture profitability by making the fish susceptible to disease.
from
https://www.researchgate.net/profil...es-of-Liver-in-Overfed-Young-Nile-Tilapia.pdf
or
Zang, L., Shimada, Y. & Nishimura, N. Development of a Novel Zebrafish Model for Type 2 Diabetes Mellitus.
Sci Rep 7, 1461 (2017).
https://doi.org/10.1038/s41598-017-01432-w
Abstract
Obesity is a major cause of type 2 diabetes mellitus (T2DM) in mammals. We have previously established a zebrafish model of diet-induced obesity (DIO zebrafish) by overfeeding
Artemia. Here we created DIO zebrafish using a different method to induce T2DM. Zebrafish were overfed a commercially available fish food using an automated feeding system. We monitored the fasting blood glucose levels in the normal-fed group (one feed/day) and overfed group (six feeds/day) over an 8-week period. The fasting blood glucose level was significantly increased in DIO zebrafish compared with that of normal-fed zebrafish. Intraperitoneal and oral glucose tolerance tests showed impaired glucose tolerance by overfeeding. Insulin production, which was determined indirectly by measuring the EGFP signal strength in overfed
Tg(−1.0ins:EGFP) sc1 zebrafish, was increased in DIO zebrafish. The anti-diabetic drugs metformin and glimepiride ameliorated hyperglycaemia in the overfed group, suggesting that this zebrafish can be used as a model of human T2DM. Finally, we conducted RNA deep sequencing and found that the gene expression profiling of liver-pancreas revealed pathways common to human T2DM. In summary, we developed a zebrafish model of T2DM that shows promise as a platform for mechanistic and therapeutic studies of diet-induced glucose intolerance and insulin resistance.
from
https://www.nature.com/articles/s41598-017-01432-w