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D-4 What Causes Insulin Resistance
Many factors can cause insulin resistance. Among those factors, the excess fat accumulates in our body, especially in the belly around and internal organs that causes insulin resistance.
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Explain the above picture: This is a process of an inflamed fat cell broken.
Step 1 - Normal fat cell. Step 2 - Swollen fat cell.
Step 3 - Inflamed fat cell. Step 4 - Ruptured fat cell.
Macrophages are cells in the blood that engulf cellular debris from damaged and broken cells. Cells in adipose tissue can swell and break when chronically fat over-fed, triggering a low grade inflammation that reduced the ability of insulin to function properly. became insulin resistance.
Think insulin as an escort for glucose that tells cells in tissues all over the body: "Glucose is available in the blood, would you like to take some inside?” - From “Mastering Diabetes”.
When insulin knocks the door of cells in tissues all over the body, they are given the opportunity to import glucose from blood. Since insulin’s job is escort glucose into tissues, when cells cannot recognize insulin well, they reject it, then glucose gets trapped in blood, causing high blood glucose. The pancreas release more insulin in the Hope of cells to import more glucose.
What causes cells reject insulin? ( insulin resistance)
The causes of insulin resistance are many factors:
1. Amount and types of food intake.
2. Activities and movement patterns.
3. Smoking or drinking alcohol..
4. The nutrient density of diet - macronutrient ratio ( carbs- to-fat-to-protein)
5. Age, genes, family diabetes history, some medicines and diseases, environmental pollutions, etc.
“Insulin resistance is caused by the accumulation of excess fat in tissues that are not designed to store large quantities of fat” - says in the “Mastering Diabetes” book.
Fat insulin connection steps:
Step 1 - Fat enters blood before glucose.
When people eat foods containing fat of soluble nutrients ( including triglycerides, phospholipids, and cholesterol). It go to stomach and stay a longer time for digestion and become chylomicrons that go to intestine to be absorbed into lymphatic system slowly, and protein digestion are slowed. The result is that fat-rich chylomicrons appear in blood more rapidly than glucose and amino acids.
Step 2. Fat enters blood and tissues.
Fatty acids enter cells easily than glucose, because fatty acids are without requiring insulin as escort. The triglycerides combined with protein in the liver to be lipoprotein which easily transport in blood and enter tissue without insulin, tissues( liver, muscle, and adipose) have no choice to absorb fatty acids in large amount.
Step 3. Fat enters adipose tissues.
Fat tissues locate in many places. The fatty acids are stored in adipose for storing energy and protect organs. But excess fat, especially the deep abdominal fat around and internal organs that increases insulin resistance, then get many chronic diseases, like obesity, diabetes, hypertension, cardiovascular disease, chronic kidney disease, fatty liver disease, stroke, cancer, etc.
Step 4. Adipose tissue becomes inflamed.
When people get high-fat diet, large quantities of fat in adipose, but it cannot expand indefinitely. If fat cells are chronically over-fed, they become inflamed, the low grade chronic inflammation that triggers insulin resistance, overtime adipose tissue can burst open, spilling their debris out into blood, it’s neighboring cells release stress cytokines ( a stress signal) into blood that let macrophages invade the tissue and engulf debris, this cytokines also trigger chronic inflammation and adipose tissue insulin resistance.
Step 5. Fat causes insulin resistance in muscle and liver.
Muscle and liver are designed to use glucose as primary energy and generate ATP (stores high energy) from glucose, and can store small amount of fat in lipid droplets and store glucose as glycogen. When muscle and liver uptake fatty acids from blood, also up-regulate enzymes in fatty acids metabolism and down regulate enzymes in glucose metabolism, fatty acids are predominant fuel which block glucose from entering cells through down-regulating insulin receptors located on the cell surfaces.
Within 2-6 hours of a single high-fat meal, insulin receptors become less functional, perform less work and difficult time recognizing insulin in the blood. This dysfunctional insulin receptors keep glucose outside of cells, leaving glucose trapped in blood for a long time, blood glucose high although not eat much carbohydrates, because muscle and liver have already accepted fatty acids as their primary energy source. First come, first served.
Step 6. Pancreas beta cells get stressed
Beta cells make up less than 1% of total pancreas weight. Beta cells are particularly sensitive to fatty acids because they have a limited ability to protect themselves against damage when they exposed in high fat concentrations for longer period of time, their antioxidant self defense mechanism are inadequate to protect them against dysfunction.
An increasing demand for insulin forces beta cells to produce insulin in overdrive increase more cellular stress that let beta cell suiside through apoptosis or programmed cell death, insulin production rapidly falls below physiological levels within a short time.
Autopsies have revealed that in majority of patients with type 2 diabetes more than half of beta cells have died. After age 20 body stop making new beta cells, therefore beta cells death is irreversible.
If you significantly reduce whole body insulin resistance can the remaining beta cells to produce enough insulin to meet the demands of all tissues? The answer is almost, always YES! The remaining beta cells are often capable of producing sufficient insulin for all tissues, but only you take steps to reduce body’s insulin needs by increase insulin sensitivity.
The “Mastering Diabetes” method teaches people how to prevent and reverse the accumulation of excess fat in non- fat tissues and prevent beta cells are subsided before it has the chance to begin its function.
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D-4 甚麽引起胰岛素抵抗？
许多因素可引起胰岛素抵抗，其中，过多的脂肪堆积在人体内，尤其是腹部脏器內和周围的脂肪，可引起胰岛素抵抗。
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图解：这是一个发炎的脂肪细胞破裂的过程。
第一步：一个正常的脂肪细胞。 第二步：这个脂肪细胞肿胀。
第三步：这个脂肪细胞发炎。 第四步：脂肪细胞破裂。
当胰岛素敲击全身组织细胞的门时，给予组织细胞从血中摄入葡萄糖的机会，因为胰岛素的工作是护卫葡萄糖进入组织细胞。当细胞不认识胰岛素时就拒绝它，使葡萄糖陷入血中，引起高血糖。这时，胰岛B 细胞释放更多的胰岛素，希望细胞摄取多量的葡萄糖。
甚麽使细胞拒绝胰岛素？（甚麽引起胰岛素抵抗？）
引起胰岛素抵抗有许多因素，如下：
食物摄入的量和类型。
运动和活动的方式。
吸烟或饮酒。
饮食的营养密度 - 大分子营养物的比例 （碳水化合物：脂肪：蛋白质）。
年龄，基因，糖尿病家族史，有些药物和疾病，外环境污染等。
“胰岛素抵抗是因过多的脂肪堆积在组织内，这些组织不是设计为储存大量脂肪用的。” - 这是在《控制糖尿病》一书里写的。
脂肪 - 胰岛素联系步騶如下：
第一步：脂肪比葡萄糖先进入血中。
当人们食入含有脂肪的食物时，可溶性脂肪（甘油三酯，磷脂，胆固醇），进入胃中进行消化，停留时间较长，并形成乳糜微粒进入小肠被吸收后，较慢地进入淋巴系统。蛋白质的消化也较慢。结果是富含脂肪的乳糜微粒快速地进入血液，比葡萄糖和氨基酸入血快得多。
第二步：脂肪进入血液和组织。
脂肪酸进入细胞比葡萄糖容易，因为脂肪酸不需要胰岛素的护卫。甘油三酯已在肝脏里和蛋白质结合成为脂蛋白，便于在血中运输。脂蛋白进入血中和组织中也不需要胰岛素。组织（肝脏，肌肉，脂肪组织）毫无选择地吸收大量的脂肪酸。
第三步：脂肪进入脂肪组织。
脂肪组织位于许多部位。脂肪酸储存在脂肪组织内，为了储存能量和保护脏器。但是，过多的脂肪，尤其是深藏在腹部脏器內和周围的脂肪，可增加胰岛素抵抗，从而引发多种慢性病，像肥胖，糖尿病，高血压。心血管病，慢性肾病，脂肪肝病，脑中风，和癌瘤等。
第四步：脂肪组织发炎。
当人们食入高脂类饮食，大量的脂肪堆积在脂肪组织内，但是，脂肪组织不能无限制地扩大，如果脂肪细胞逐渐地扩大，它出现炎症，这个低度的慢性炎症可诱发胰岛素抵抗，长时期后，脂肪组织会肿胀破裂，其碎片进入血液，它的邻居细胞释放紧张细胞因子（stress cytokines)进入血液，使得巨噬细胞侵入组织去吞噬细胞碎片。这些细胞因子可引起慢性炎症反应，也使脂肪组织出现胰岛素抵抗。
第五步：脂肪引起肌肉和肝脏的胰岛素抵抗。
肌肉和肝脏是设计为用葡萄糖作为首要的能源，同时从葡萄糖代谢产生ATP（三磷酸腺苷酸，是高能化合物），只能存储少量油滴的脂肪。肌肉和肝脏的葡萄糖以糖原形式储存。当肌肉和肝脏从血中摄取脂肪酸，也调高了脂肪酸代谢的酶活性，同时调低了葡萄糖代谢的酶活性，脂肪酸成为优先的能源，同时阻断了葡萄糖进入细胞，这是通过调低细胞表面的胰岛素受体实现的。
在吃一顿高脂肪饭2-6小时内，胰岛素受体的功能降低，完成很少的工作，难于辨认血中的胰岛素。这个功能失调的胰岛素受体，使葡萄糖在细胞外，陷于血中长时间，虽然没有食入多少碳水化合物。因为，肌肉和肝脏已经接受脂肪酸作为他们的首要的能源。先来后到。
第六步：胰脏B细胞紧张起来。
B细胞只组成胰脏总重量的少于1%，B细胞对脂肪酸特别敏感，因为B细胞有限的防伤害的能力。当它们长时间暴露于高浓度的脂肪中，它们的抗氧化防卫机制，不足以防御它们不失去功能。
由于对胰岛素的需求，迫使B细胞生产过多的胰岛素，以致B细胞疲惫紧张，到自杀，经过细胞凋亡或细胞死亡程序。此时在短时间内，胰岛素的产量急剧下降到生理水平以下。
尸体解剖揭示，多数的2型糖尿病人已有半数的B细胞死亡。人体在20岁即停止生成新的B细胞，因此， B细胞的死亡是不能逆转的。
如果你已经降低全身的胰岛素抵抗，能使已存的B细胞生产出足够供给全体组织的需要量吗？
答案是 - 几乎总是！已存的B细胞经常是有能力给所有的组织生产足够的胰岛素，但是，你必须采取行动，通过提高胰岛素的敏感性，以降低身体对胰岛素的需求。。
《控制糖尿病》方法教给人们，如何避免和逆转过多脂肪堆积在非脂肪组织，和防止B细胞的继续损伤和自杀，使它有机会开始它的功能。
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