The Antisteatotic and Hypolipidemic Effect of Insect Meal in Obese Zucker Rats is Accompanied by Profound Changes in Hepatic Phospholipid and 1‐Carbon Metabolism

Abstract

Scope The hypothesis is tested that insect meal, which has a low methionine content, reduces the hepatic phosphatidylcholine (PC):phosphatidylethanolamine (PE) ratio, which is a critical determinant of hepatic lipid synthesis, by decreasing availability of the methionine metabolite S‐adenosylmethionine (SAM). Methods and results Obese rats (n = 24) are randomly divided into two groups (Obese Casein and Obese Insect) of 12 rats each. In addition, lean rats (n = 12) are used as control group (LC). Groups LC and OC receive a control diet with casein as protein source, whereas in the OI group, casein is replaced isonitrogenously by insect meal, which is found to be less digestible (–12% units). Plasma and liver concentrations of lipids and hepatic expression of lipid synthesizing genes are reduced in the OI group compared to the OC group. Plasma and liver concentration of PC and the PC:PE ratio are decreased in the OI group compared to the OC group, while hepatic concentration of SAM and the hepatic SAM:S‐adenosylhomocysteine (SAH) ratio is lower in the OI group than in the OC group. Conclusion The decrease of the hepatic PC:PE ratio is probably a key mechanism explaining the pronounced antisteatotic and hypolipidemic action of insect meal in obese rats.

Comprehensive evaluation of the metabolic effects of insect meal from Tenebrio molitor L. in growing pigs by transcriptomics, metabolomics and lipidomics

“…This assumption is also justified when considering the results obtained from lipidomics of liver and plasma of the pigs. In contrast to our recent studies in obese Zucker rats [15,16], inclusion of IM into the diet had no effect on TG and cholesterol concentrations in plasma and liver of the pigs. However, the lack of a TG-and cholesterollowering effect as observed in obese Zucker rats, which exhibit severe hyperlipidemia and liver steatosis when compared to lean rats, is not surprising because physiologically normal levels of lipids in plasma and liver as found in young and metabolically healthy pigs are unlikely to be further reduced by dietary interventions.…”

“…An increased hepatic PC:PE-ratio of greater 2 is considered critically [17], because it has been linked with the development of fatty liver disease [56,57]. Despite the slight increase (+ 5%) of the hepatic PC:PE-ratio in pigs of group IM10 was statistically significant, we postulate that this increase is not of biological relevance considering the marked elevation (+ 35%) of the hepatic PC:PE-ratio in severely steatotic obese Zucker rats compared with non-steatotic lean Zucker rats [16]. In line with our assumption, there was no indication of fatty liver induction as evident from the observation that hepatic TG concentrations of the pigs of all groups were within the physiological range reported from others [58,59].…”

“…Dry matter content, energy content and concentrations of crude nutrients and amino acids in the diets and the IM were determined by official methods [21,22]. The chitin content of the insect meal was determined as described recently [16].…”

“…We have recently demonstrated for the first time in two studies with genetically obese rats that IM produced from larvae of the yellow mealworm (Tenebrio molitor L.) has remarkable effects on lipid metabolism, such as attenuation of liver steatosis and decrease of hyperlipidemia, − effects which are likely explained by the profound inhibition of hepatic lipid synthesis observed in these studies [15,16]. Inhibition of hepatic lipid synthesis is possibly mediated by the marked modulation of hepatic phospholipid metabolism [e.g.…”

“…Inhibition of hepatic lipid synthesis is possibly mediated by the marked modulation of hepatic phospholipid metabolism [e.g. decrease of hepatic phosphatidylcholine (PC) to phosphatidylethanolamine (PE) ratio] in the obese rats fed the IM [16], because the hepatic PC:PE ratio is a critical determinant of hepatic lipid synthesis [17]. Apart from these modulatory effects on lipid metabolism, largely unexplained effects of IM in the obese rat model were found using screening techniques, such as transcriptomics and metabolomics, on several other metabolic pathways, like metabolism of amino acids and xenobiotics and cellular stress response [15], overall indicating a multifaceted influence of IM on intermediary metabolism of rodents.…”