The fats (fatty acids) are first cut in small pieces by the enzyme HSL (hormone sensitive lipase). Under the influence of HSL they can leave the cell and travel via the circulation which carries them to muscles and tissues to be burned to make energy ATP (adenosine triphosphate). However, this only occurs if blood sugar levels are normal and insulin production is moderate and in the normal healthy range. This makes muscles very happy because they prefer to burn fats for energy over carbs. In health, muscles repair and grow at night if we eat to support circadian rhythm. A water only fast of 14 to 18 hours at night while we sleep makes us strong! Fat gets burned and muscles are strengthened while we sleep.
High insulin production in response to excess carbohydrate intake and/or prolonged eating raises insulin levels (2030). The fats we eat are as important as the carbohydrates that we eat in contributing insulin resistance and metabolic syndrome, the precursors of type 2 diabetes. Yam D, et al, “The Israeli Paradox” Isr J Med Sci. 1996 (864), Meta-analysis, de Souza R et al, BMJ 2015 (1178) and (681, 1121, 1244-1248, 2258, 2263)
Cooking with vegetable oils (for example soy oil) raises blood sugar levels (864, 1121, 1224-1248, 2263) provoking overproduction of insulin. Industrial trans fats appear to alter cell wall structure and insulin receptor activity making cells resistant to insulin. In turn the high insulin levels in the blood inhibit the enzyme HSL (Hormone Sensitive Lipase). The high insulin levels shut the “HSL door” of the fat cell so fats cannot leave the fat cell to be burned. Meanwhile more fats are made from the sugar (carbohydrates) in the liver and the fats then travel via the blood circulation to fat cells where they enter the fat cells for storage. The result is weight gain as fat.
Natural trans fats (trans-palmitoleic acid) found in cream, whole milk, butter and unprocessed red meat reduce risk of type 2 diabetes. (1178)
Ultimately, the poor tired pancreas beta cells cannot keep up with the effect of vegetable oil, trans fats, and excess carbohydrate intake, high sugar impact carbs, and/or prolonged eating.
In exhaustion the pancreas produces a little less insulin, but it still makes enough insulin for insulin levels to remain above the healthy level and to shut down HSL enzyme activity. This “shuts the door” of fat cells and fats are not able to leave the fat cells and be burned for energy.
Fats (fatty acids) continue to enter the fat cells to be stored.
The result of the final step in developing insulin resistance remains the same, weight gain as fat.
In health, muscles prefer to burn fats over carbs (sugar) for their energy source. Fats are the more efficient fuel for muscles to burn to make ATP energy. Muscles do burn some limited amounts of carbs (sugar) to generate energy (ATP), but it is not their preferred and primary source of energy. When low sugar impact carbs are eaten in healthy amounts in a 6 to 10 hour eating window, muscles remain very sensitive to insulin and carbs (sugars) can readily leave the blood and enter muscle cells to be burned.
Muscles are like team players and are willing to help the body out if too many carbohydrates are eaten occasionally. Muscles are like switch hitters on a baseball team that can bat either left handed or right handed to help the team out. If too many carbs are eaten on occasion, muscles will switch and burn carbs for energy for a temporary period to help lower the blood sugar back toward normal.
The pancreas has a job of its own. The goal of the pancreas is to make enough insulin to keep the blood sugar level normal. This is an easy job if healthy carbohydrates are eaten at the right times.
All carbs eaten are converted to sugars in the body. Over time, if excess carbohydrate abuse continues, the muscles begin to resist the excess sugar load. It is like they are saying “Hey we already have too much sugar over here, don’t send any more.” Blood sugar levels rise. The pancreas knows high blood sugar levels are unhealthy and overrides the resistance of the muscles to sugar by generating lots of insulin to bulldoze the sugar into the muscles despite their resistance to insulin and resistance to sugar intake. In stage 1 of insulin resistance, the still healthy pancreas Beta cells swell, grow, and produce lots of insulin to process the extra sugars from the excess carb intake and/or prolonged eating window.
High insulin production raises insulin levels that in turn inhibits the enzyme HSL (Hormone Sensitive Lipase). That is why it is called hormone sensitive lipase, because it is sensitive to how much insulin hormone is in the blood. High insulin levels shut down the activity of HSL thus preventing the burning of fats. Fats no longer leave the fat cells and travel to muscles to be burned by muscle cells. Instead, sugar enters muscles and fats enter the fat cells. Intake of vegetable oils (omega-6 oils) and trans fats also results insulin resistance. Meta-analysis, Ramsden CE, et al, Br J Nutr. 2010 (934) and (864)
In the final stage of insulin resistance, the swollen pancreas Beta cells eventually become exhausted from being over worked; they shrink and produce less insulin, but it is still more insulin than the normal healthy insulin level and is enough to keep blocking HSL (hormone sensitive lipase) from working. Therefore, fats are locked in fat cells and cannot be released and sent to muscles to burn for energy. However, not quite enough insulin is made to push all the excess sugar out of the blood and into muscle cells.
This combination makes muscles waste away because they are deprived of their primary energy source fats, and at the same time they are resistant to their backup energy source sugar. Blood sugar rises leading to metabolic syndrome, prediabetes, type 2 diabetes, and weak muscles. Frailty is a complication of metabolic syndrome and muscle wasting. The fat cells continue to store fats secondary to intake of vegetable oils, prolonged eating, and/or excess carbohydrate intake. High insulin levels slam the HSL fat exit door of the fat cells shut, so fats cannot leave fat cells. Meanwhile, fats continue to enter the fat cells. Muscles are deprived of energy from fats and waste away.
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Almost twice as much food was eaten at the next meal if the person had a high-carb low-fat meal at the previous meal. (807) Dr. David Ludwig, Professor of Pediatrics at Harvard, and Children’s Hospital in Boston.
Excess carbohydrates (and sugars) we eat are converted by the liver to triglycerides (fats) and cholesterol.
People who eat too many carbohydrates (carbs) can develop “fatty livers” because excess carbohydrates are converted to fat (triglycerides TG or fatty acids FA) in the liver. The fatty liver tissue is seen if a liver biopsy is taken. “Fatty liver disease” is usually a reversible condition. Large globules of triglyceride fat accumulate in liver cells. In the late stages, the size of the fat globules increases, pushing the nucleus to the edge of the cell. If the condition persists, large fat globules may come together (coalesce) and produce fatty cysts, which are irreversible lesions that can damage the liver.