Hnf4^Δ17/Hnf4^Δ33 larvae exhibit an abundant progenitor pool coupled with the reduction in differentiated cells in the lymph gland primary lobe.

Vast majority of Hnf4^Δ17/Hnf4^Δ33 heterozygotes fail to eclose and the rest die as young adults - none survive past post-eclosion day 1 when raised on standard lab diet.

Hnf4^Δ17/Hnf4^Δ33 heterozygotes are hyperglycemic and sugar intolerant: the percentage of animals able to eclose as well as the adult life-span is significantly improved by lowering the levels of dietary sugar (the lower the dietary sugar, the better the eclosion and adult survival rates).

Hnf4^Δ17/Hnf4^Δ33 heterozygote adults show fragmented mitochondria phenotype in the fat body.

Hnf4^Δ17/+ suppresses position effect variegation at the w locus caused by P{SUPor-P}KV00108.

Hnf4^Δ17/Hnf4^Δ33 transheterozygous mutants maintained under normal culture conditions progress through development until adult eclosion, when many of the animals die with their head protruding from the pupal case. The remaining mutant adults die within a day of eclosion. Maintaining these mutants at low density under ideal culture conditions however, results in many animals surviving this lethal period and developing into morphologically normal adults. This dependence of Hnf4^Δ17/Hnf4^Δ33 mutant lethality on culture conditions suggests that the phenotype arises, at least in part, from metabolic defects due to the nutritional status of the animal. Whereas most control larvae survive for 2 days in the absence of nutrients, almost all Hnf4^Δ17/Hnf4^Δ33 mutants succumb during this period. However, Hnf4^Δ17/Hnf4^Δ33 mutants retain the ability to survive on a sugar diet.

Levels of glycogen and triglycerides do not change significantly in fed Hnf4^Δ17/Hnf4^Δ33 transheterozygotes compared to controls. Starved Hnf4^Δ17/Hnf4^Δ33 mutants however, have significantly higher levels of triglycerides compared to starved control larvae. Starvation induced autophagy is induced normally in Hnf4^Δ17/Hnf4^Δ33 mutant larvae.

After 1-day of starvation, lipids are effectively cleared from the midgut of control animals and accumulate in the oenocytes. Higher levels of lipids, however, are evident in the midguts of starved Hnf4^Δ17/Hnf4^Δ33 mutants compared to starved controls. Slightly elevated lipid levels are seen in the midguts and oenocytes of fed Hnf4^Δ17/Hnf4^Δ33 mutants relative to fed controls, suggesting that metabolic dysfunction is also present in the fed state. Fed Hnf4^Δ17/Hnf4^Δ33 mutants have essentially normal lipid droplet morphology. These droplets however, appear to aggregate abnormally in starved mutants.

Starved Hnf4^Δ17/Hnf4^Δ33 mutants display reproducibly increased levels of free long chain fatty acids compared to controls.