Lentils are pulses, a.k.a. the dry edible seeds of certain crops (like beans, chickpeas, and peas). Pulses are just everywhere these days because they’re packed with plant-based protein and fiber, not to mention antioxidants, minerals, and B vitamins. All of those compounds help protect you from plaque buildup while optimizing blood flow and assisting your body in efficiently using the nutrients you consume.
In humans, diets high in saturated fat and cholesterol raise HDL-cholesterol (HDL-C) levels. To explore the mechanism, we have devised a mouse model that mimics the human situation. In this model, HuAITg and control mice were studied on low fat (9% cal)-low cholesterol (57 mg/1,000 kcal) (chow) and high fat (41% cal)-high cholesterol (437 mg/1,000 kcal) (milk-fat based) diets. The mice responded to increased dietary fat by increasing both HDL-C and apo A-I levels, with a greater increase in HDL-C levels. This was compatible with an increase in HDL size observed by nondenaturing gradient gel electrophoresis. Turnover studies with doubly labeled HDL showed that dietary fat both increase the transport rate (TR) and decreased the fractional catabolic rate of HDL cholesterol ester (CE) and apo A-I, with the largest effect on HDL CE TR. The latter suggested that dietary fat increases reverse cholesterol transport through the HDL pathway, perhaps as an adaptation to the metabolic load of a high fat diet. The increase in apo A-I TR by dietary fat was confirmed by experiments showing increased apo A-I secretion from primary hepatocytes isolated from animals on the high fat diet. The increased apo A-I production was not associated with any increase in hepatic or intestinal apo A-I mRNA, suggesting that the mechanism of the dietary fat effect was posttranscriptional, involving either increased translatability of the apo A-I mRNA or less intracellular apo A-I degradation. The dietary fat-induced decrease in HDL CE and apo A-I fractional catabolic rate may have been caused by the increase in HDL particle size, as was suggested by our previous studies in humans. In summary, a mouse model has been developed and experiments performed to better understand the paradoxical HDL-raising effect of a high fat diet.
I had a minor stroke in October 2017, since then I have gained 15 pounds. I have tried everything (exercising included),, and I am not loosing any weight . I take 1 pill everyday to lower my cholesterol. I hate this weight around me, and is mentally affecting me as I have been slim for last 8 years. None of my clothes fit me … Any suggestions will be appreciated…
How much do you know about your cholesterol? You probably know that there are two different kinds – high-density lipoprotein (HDL), which is the “good” cholesterol, and low-density lipoprotein (LDL), also known as the “bad” cholesterol. High HDL levels help carry cholesterol from your arteries to your liver and also possess antioxidants and anti-inflammatory properties, which are linked to a reduced risk of heart disease.
Hyperalphalipoproteinemia (HALP) may be familial, including primary (without CETP deficiency) and otherwise (with CETP deficiency), or secondary.  Familial HALP (aside from the primary form) is a well-documented genetic form of hypercholesterolemia characterized by a deficiency of CETP, a key protein in the reverse cholesterol transport (RCT) system that facilitates the transfer of cholesteryl esters from high-density lipoprotein (HDL) to beta lipoproteins. Primary HALP is a term used for familial elevated HDL cholesterol levels that are not due to CETP deficiency and for which the cause is unknown. Secondary HALP is due to environmental factors or medications.