關於 triglycerides in liver ，我們在網路上蒐集到這些相關的討論、資訊與評價

NOT ALL FRUITS ARE CREATED EQUAL. Refer to this chart and opt for fruits which are lower in fructose like citrus fruits, guava (not shown), chilies (yes it's a fruit) and avocado✅
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Limit or even cut off high fructose containing fruits like grapes, lychee, apples etc if you are having high triglycerides (lipids/blood fat), sub-par liver or kidney function, high uric acid or if you have high levels of visceral fat or body fat📈
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In continuation from my IGTV latest post, fructose is highly lipogenic (fat & triglycerides producing). It produces 50% more triglycerides than glucose😱
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Fructose does not have a high glycemic index. It will NOT stimulate insulin, leptin (suppress appetite), suppress ghrelin, nor stimulate thermogenesis BUT it's metabolized directly by the liver into lipids (triglycerides)❗
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Of cause, synthetic man-made fructose which is high fructose corn syrup (HFCS) found in soft drinks & junk food are worse compared to fruits. But if you are following a diet high in sweet fruits consumption and drinking lots of fruit juices its can be as damaging‼
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So if you know someone who does not eat alot of food and they say they only take plenty of fruits and fruit juice but still has high body fat, perhaps this could be the reason. It's not about the calories. It's how your food is metabolized and stored♻️
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Having a blood review, body composition check & dietary assessment with a Nutrition Medicine practitioner will help to identify the root cause of your issue📋

不能胖才是大麻煩

Adipose tissue grows by two mechanisms: hyperplasia (cell number increase) and hypertrophy (cell size increase).

We all have a genetic predisposition to the amount of fat mass that we can safely achieve..Some folks have a very limited ability to recruit new adipose cells to store excess lipids in the subcutaneous adipose tissue. The recruitment of new adipose cells is known as Adipogenesis.

Adipogenesis is the process of cell differentiation by which pre-adipocytes become adipocytes. Once these folks can no longer recruit new adipose cells to store excess lipids during times of over-feeding, their existing adipocytes (fat cells) in their fat mass, their adipocytes grow in cell size and they reach a point where they become hypertrophic.

Their adipocytes (fat cells) become very inflamed, very insulin resistant. They start leaking all kinds of inflammatory markers into the circulation. These adipocytes (fat cells) become so insulin resistant that they can no longer properly regulate the flow of fatty acids and glycerol from storage. There is an excess spill-over of fatty acids to the liver. These excess fatty acids are re-esterfied in the liver to triglycerides. These excess fatty acids and triglycerides cause extreme insulin resistance in the liver. They also cause fatty liver. There is a dramatic rise in circulating triglycerides (lipids). These excess lipids also end up stored in the pancreas and other organs causing lipotoxicity. Welcome to T2 diabetes.

"Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death. The tissues normally affected include the kidneys, liver, heart and skeletal muscle. Lipotoxicity is believed to have a role in heart failure, obesity, and diabetes, and is estimated to affect approximately 25% of the adult American population."
https://en.wikipedia.org/wiki/Lipotoxicity .

Folks that have metabolically health fat mass have adipose tissue that grows by hyperplasia, increase in cell number..

Adiponectin is a very important hormone that is secreted by our adipose tissue..Adiponectin is very insulin sensitizing...also increases our metabolic rate...increases fatty acid oxidation...preserves pancreatic beta-cells...adiponectin promotes glucose-stimulated insulin secretion (GSIS), prevents apoptosis (cell death), and enhances the viability of pancreatic beta-cells under a variety of conditions.

Once you have dysfunctional adipose tissue, your adipocytes release LESS adiponectin and more leptin..Adiponectin is very anti-inflammatory...Leptin is very PRO-inflammatory.

LOW blood adiponectin levels are VERY indicative of T2 diabetes and fatty liver, many other diseases.

Small healthy fat cells release very high levels of adiponectin, very low levels of leptin..

I would need to try and write a few posts about adiponectin, T2D and fatty liver..

Here is a good article on adiponectin:

"Ever since its initial discovery, adiponectin has inspired widespread interest. Readily detectable in blood, stable upon collection and relatively inert to the method of collection and diurnal changes, its levels inversely correlate with multiple metabolic disorders and related diseases. Adiponectin can therefore serve as a potent clinical biomarker in humans and rodents. From the 10,000 studies over the past two decades since its discovery, it is widely appreciated that adiponectin exerts pleiotropic metabolic effects. Adiponectin sensitizes peripheral tissues to insulin and protects against inflammation and apoptosis."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773837/ .

Biggest Nutrition and Food Myths Busted

“High-Fructose Corn Syrup (HFCS) is worse for you than sugar.”
Though consumers who fill their shopping carts with products labeled “No HFCS” might feel otherwise, the idea that high-fructose corn syrup is any more harmful to your health than sugar is “one of those urban myths that sounds right but is basically wrong,” according to the Center for Science in the Public Interest, a Washington, D.C.-based nutrition and health advocacy group.

High-fructose corn syrup was created to mimic sucrose (table sugar), so its composition is almost identical to sucrose’s (55 percent fructose, 45 percent glucose; with sucrose the ratio is 50:50). Calorie-wise, it’s a dead ringer for sucrose. And in studies that compare the effects of HFCS with other sweeteners, HFCS and sucrose have very similar effects on blood levels of insulin, glucose, triglycerides and satiety hormones. In short, it seems to be no worse—but also no better—than sucrose, or table sugar.
“The debate about HFCS and sucrose [table sugar] is taking the focus off the more important question,” says Kimber Stanhope, Ph.D., R.D., a researcher at the University of California, Davis, who has studied the sweetener extensively. “What we should be asking is ‘What are the effects of all sugars (HFCS and sucrose) in the diet?’”

Epidemiologic studies show that consuming large amounts of added sweeteners—primarily in sodas and other sweetened drinks—is associated with greater risk of fatty liver disease, insulin resistance, heart disease and type 2 diabetes. And it’s not just the extra calories they provide that may be hurting us; research by Stanhope and others suggests that fructose itself in added sugars may be hazardous to our health too. One problem is that our bodies weren’t designed to handle a large amount of fructose at a time, she notes, because we wouldn’t have come across it in our food supply. “If you look at what nature provided for humans to eat, we only had fructose in whole fruit, in amounts that are relatively dilute.” Problems arose when we learned how to turn foods—which contain fiber, water and other nutrients—into pure sources of sugars (e.g., refining sugarcane into table sugar).

But the associations between sweetener consumption and disease don’t implicate just HFCS, which despite its name contains only a little more fructose than sucrose does, Stanhope emphasizes. It’s the sheer amount of the sweet stuff we consume that matters or, to put it another way, it’s the dose that is the problem. Too much honey, agave syrup or dehydrated cane juice would likely cause the same health problems.

“The American Heart Association recently recommended that women consume no more than 100 calories a day in added sugars [6 teaspoons]; men, 150 calories [9 teaspoons],” Stanhope notes. Our current intake, however, hovers around 355 calories per day. “The U.S. population isn’t anywhere close to [the AHA’s] goal.”