I have conducted a feeding trial on an aquaculture(d) organism and analysed the results for total lipid, total protein, lipid classes, and fatty acids.The results show that the diets likely caused a nutritional overload of the digestive system, being too high in both protein and lipid, and there is a strong correlation with high lipid and low growth.
The lipid component of the diet was largely neutral lipids, and I have found several studies describing the growth-depressing effect of an over-supply of neutral lipids. However, these studies show that an over-supply of neutral lipids leads to increased deposition of neutral lipids, largely in the form of triacylglycerol (TAG). In my results, the organisms fed the high-lipid diets have deposited huge amounts of phospholipids, and contain very little TAG.
Generally large amounts of structural lipids in a stressed animal would indicate catabolism of storage lipids for energy, but this would also lead to lowered total lipid. In my case, I have very high total lipid concentrations.
If anyone could float some ideas as to why this might be the case I would really appreciate it. Thanks
When you state you observe deposition of huge amounts of phospholipids (PL), do you mean you observe large large accumulation of PL relative to total body mass, or total protein? And could you determine if the PL increase was extracellular or intracellular?
Depending on the specifics, increased PL could correlate with increased organism size, or specific organs within the animal. Or perhaps increased subcellular organelles such as microsomes.
I think that better results can be achieved in terms of growth, survival and development, when-this is the case of fish culture systems -fishes and larvae are fed with different levels of EPA and DHA in the PL fraction of the diet.This to avoid steatosis or to aid functional organization and maturation of the alimentary system
Thank you both for the answers. Lawrence, there was a large accumulation of PL relative to other lipid classes, as well as total body mass. I cannot determine if it is intra- or extra-cellular.
It is not due to higher growth because the animals with the highest total lipid/total PL grew the least. Thus, it appears to be a stress response. I'm just not sure how/why this resulted in large deposition of PL.
Cheers
Hi Jessica,
Do you know what specific PLs are increasing? Is it a universal increase or just one specific class? Wondering if it's also connected to the high protein diet.
Hi Simon, thanks for your answer. It was all the PLs, although I would say phosphatidylethanolamine (PE) and phosphatidylserine/phosphatidylinositol (PSPI) and phosphatidylcholine (PE) were predominant. I have also been considering the high protein as a factor. Do you know what lipid classes are deposited after protein deamination? Or perhaps it depends on the amino acids.
Cheers
Jess
I am no expert in biichemistry or physiology, but can float ideas, useful or not.t have you made connections with human stress- induced problems of localisation? Too much, probably in the wrong place, and low growth reminds me of human sarcopenia and ACh niot in the right place.
"too much" survival/'vitality' can lead to suppression of entire systems; example ; too much survival (sympathetic activation) can suppress parasympathetic and so basic viability function. Other example: sugar & diabetes.
I am a fish neurobiologist.But I know that in the experimental designs for culture systems the dietary HUFA have been suggested as dietary components for marine fish growth, survival, and activity of some digestive enzymes.As for SNS I know it, as regulator of TG metabolism,mediates the effects of hormones on the peripheral TG metabolism.
To answer your second question Jessica, I'm not sure if there would be specific phospholipid classes enriched above others. Is there a high protein content in the diet? The high nitrogen content of the proteins could enhance the phospholipids for sure, the head groups of PS, PE, PC and the sphingolipids (if this organism has these) can all come from serine. What is the specific aqua organism you are dealing with? Ultimately I would hypothesise that the diet is too rich so that there is no need for the organism to have many neutral lipids and a variety of the other lipids is being made instead.
Thank you to everyone for the great ideas.
Simon, the diet has very high lipid as well as protein. The organisms accumulated a lot of protein but their growth was low. Could you recommend any papers that discuss high dietary nitrogen enhancing phospholipid content?
I will reveal the mystery organism to you. It is......coral! Scleractinian coral (stony/reef building) to be more specific. :)
Hmm, I have a poem from Giacomo and a blank answer from Simon. If this is a result of the organism turning out to be coral, I can relate. Coral nutrition would drive anyone crazy.
I can't seem to post an answer, Jessica I have e-mailed you instead!
Thanks, Simon. I haven't go any emails from you? Did you send to [email protected]? Cheers :)
Calorie restriction that main¬tains the anti-aging genes changes the core body temperature and promotes species longevity. Stress and calorie consump¬tion are sensitive to Sirtuin 1 function with relevance heat shock protein 70 metabolism and mitochondrial biogenesis. Sirt 1 regulation of the circadian rhythm mediates melatonin effects on core body temperature regulation and immune responses. Diet, stress and fat are essential factors that determine species lon¬gevity with relevance to heat shock gene regulation and mi¬tochondrial disease in animals and man. Strenuous exercise to activate the cellular heat shock gene in animals and man should be carefully controlled to prevent magnesium deficien¬cy with relevance to immune disorders and mitophagy. Animals must have a functional anti-aging gene Sirt 1 to allow rapid hepatic and adipose tissue metabolism of fatty acids and glucose. REFERENCE: Martins IJ. Regulation of Core Body Temperature and the Immune System Determines Species Longevity. Curr Updates Gerontol. (2017) 1: 6.1