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Kraken
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To assess the contribution of dietary fatty acids, male and female mice fed a high-fat diet (35% energy as fat, linoleic acid:α-linolenic acid ratio of 28) were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake.
(jfl at that quote; birthweight is decreasing but bodyfat is increasing. What an utter subhuman trait)"Interestingly, body weight at birth appeared to decrease across generations, but this trend was not statistically significant"
"Abbreviations: HF0–HF4, HFD-fed mice; hf5, ω6HFD-fed fifth-generation offspring of revHF4; HFD, high-fat diet (ω6HFD); revHF1, HF1 pups fed STD diet at weaning; revHF3, HF3 pups fed STD diet at weaning; revHF4, HF4 pups fed STD diet at weaning; STD, chow diet-fed mice; std5, STD-fed fifth-generation offspring of revHF4. "
This increase in bodyweight was reduced just by reducing PUFAs by eating normal chow again. But..."The PUFA profile was not different between HF0 and HF4 mice (n = 4), showing that no further changes occurred once STD-fed mice had been switched to the ω6HFD"
"The incomplete reversal of the adipose phenotype at later generations suggested that some transgenerational memory had been acquired, allowing revHF4 mice to respond more rapidly than STD mice to the ω6HFD."
Interestingly markers of inflammation were almost normal by the 4th generation, except insulin, which indicates insulin resistance.
The PUFA-feeding also changed some genetic expression, indicating the role of Epigenetics in relation to diet/lifestyle