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Excess lipid accumulation in the arterial intima and formation of macrophage-derived foam cells in the plaque could cause atherosclerotic lesion.
Elevated levels of MDA in renal tissue have been regarded as an indicator for cellular damage due to excess lipid peroxidation processes that occur during malfunctioning of the antioxidant defence system [27].
Similarly, the increase in plasma and acrosomal membrane integrity could be attributed to higher concentrations of polyunsaturated fatty acids (a key cell-membrane component), combined with the prevention of excess lipid peroxidation by antioxidants.
Chronically increased dietary lipid supply often leads to excess lipid accumulation in the heart, which is linked to a variety of maladaptive phenomena, such as insulin resistance, cardiac hypertrophy and contractile dysfunction.
Results of flux distribution demonstrated that NADPH provided by cytosolic malic enzyme and the acetyl-CoA from cytoplasmic citrate by the ATP: citrate lyase were the two primary sources for excess lipid accumulation.
The final mixture was repeatedly centrifuged and washed in dilute PBS to remove excess lipid.
Hepatic SCD1 action actually plays a key role in the partitioning of excess lipid and enables adequate storage [26].
It is possible that timing of high-fat diet intake affects the animal's ability to handle the excess lipid.
In the context of pancreatic β-cell biology, excess lipid exposure is known to be detrimental for both β-cell function and survival [42].
To judge whether increased lipoprotein formation affect metabolism of free fatty acids in hearts with excess lipid accumulation, we quantified the expression of selected genes controlling key steps in cardiac fatty acid metabolism.
In Plutella xylostella, for example, Warbrick-Smith et al [17] demonstrated that the laboratory populations of caterpillars that were restricted to high-carbohydrate diets for multiple generations evolved the ability to reduce fat storage, whereas the initial response to those diets typically results in excess lipid storage and reduced fitness.
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