糖尿病的根本原因是胰岛素抵抗，胰岛素抵抗的原因是什么?-最重要的原因是饱和脂肪过多

What Causes Insulin Resistance? Lipid Overload

　

　

 

By Dr. Cyrus Khambatta

作者介绍

Cyrus Khambatta. 在加州大学伯克利分校获得营养生物化学博士学位，并获得斯坦福大学机械工程学士学位。他在22岁时被诊断出患有1型糖尿病，在此后的11年里，他一直在研究胰岛细胞衰竭和胰岛素抵抗。Khambatta 热衷于营养学和锻炼，通过MangoMan营养疗法和健身指导，教授逆转糖尿病的根源——胰岛素抵抗而不是治疗高血糖症状的原则，实现对血糖波动的高度控制。

 

在过去的一年里，我与成百上千的糖尿病患者进行了互动，并且学到了重要的一课，它完全改变了我对糖尿病的看法。在我的职业生涯早期，我就意识到这一点，作为糖尿病患者的营养和健身教练，我一直坚持这一观点。

 

胰岛素抵抗是与2型糖尿病相关的最常见的一个状况, 现在越来越多的证据揭示了事实, 胰岛素抵抗是许多以前认为与血糖无关的疾病,包括(但不限于)心脏病、糖尿病、动脉粥样硬化、代谢综合征、肥胖和癌症的共同主线。

 

这清楚表明: 胰岛素抵抗会显著增加你的患上心血管疾病的风险，这将大大降低你的生活质量，降低你的预期寿命。

 

观看这段视频，了解胰岛素抵抗原因的梗概:

　

https://www.mangomannutrition.com/causes-insulin-resistance-lipid-overload-2/

　

 

什么是胰岛素（INSULIN)?

胰岛素是一种激素，它是由胰腺分泌的，以应对血糖升高。当你摄入碳水化合物时，进入血液的葡萄糖会敲开胰腺细胞的门，作为制造胰岛素的信号。

　

　

 

胰岛素是打开门使葡萄糖进入人体组织的钥匙。胰岛素告诉你的细胞“Yoo hoo!”捡起这葡萄糖。到处都是。”

　

　

 

如果没有胰岛素，肝脏、肌肉和脂肪中的细胞就很难从血液中吸收葡萄糖。这些组织在没有胰岛素帮助的情况下，仅能摄取量(5-10%)的循环中的葡萄糖。当胰岛素出现时，能被输送到组织中的葡萄糖含量会显著增加，从而使组织得到适当的喂养，并使血糖浓度保持在正常范围内。系统是这样的:

 

 

 

 

什么是胰岛素抵抗？

胰岛素抵抗是人体多种组织对胰岛素（Insulin) 的作用产生抵抗的一种状态。简单地说，当组织对胰岛素反应迟钝时，就会产生胰岛素抵抗(Insulin Resistance)。

　

　

 

由于胰岛素抵抗，胰腺被迫分泌大量胰岛素，导致高胰岛素血症。

　

 

高胰岛素血症是许多组织的危险情况，仅仅是因为血液中的高胰岛素浓度是细胞生长的有力信号。更多的胰岛素意味着更多的组织生长。更多的组织生长通常会导致脂肪增加，细胞复制率增加，癌症风险显著增加。许多研究现在已经开始揭示胰岛素抵抗和癌症之间的联系，其中一项研究指出:

　

胰岛素抵抗在肥胖或2型糖尿病(T2D)患者中很常见，在这种情况下，循环胰岛素水平经常升高。最近流行病学和临床证据表明胰岛素抵抗和癌症之间存在联系。这种关联的机制尚不清楚，但高胰岛素血症(胰岛素抵抗的一个标志)和生物可用性胰岛素样生长因子I (IGF-I)的增加似乎在胰岛素抵抗患者的肿瘤启动和进展中起作用(1)。

　

　

 

科学家对胰岛素抵抗了解多少?

关于胰岛素抵抗到底是什么引起了大量的困惑，在我作为一个1型糖尿病患者的经历以及我作为一名研究科学家的职业生涯中，我开始意识到关于胰岛素抵抗的拯救生命的信息是知之甚少的。

 

在研究世界对胰岛素抵抗的理解和大众对胰岛素抵抗的理解之间存在着一堵高墙。

　

　

不幸的是，如果信息不交到需要的人手中，优秀的研究就没有什么用处。这当然是胰岛素抵抗的例子。这幅图是这样的:

 

这堵墙存在的原因有很多，并且受到经济力量的严重影响，这些经济力量从糖尿病等终身性疾病获得好处。你可能听说过“治愈疾病赚不到钱 There is no money in the cure”这句话。这是一种真实的说法，而这种做法是将拯救生命的信息传不到从需要的人手上。

 

导致胰岛素抵抗的原因是什么?

研究人员每天都在孜孜不倦地讨论胰岛素抵抗的因果机制，每天都要跋涉数千英里去参加大型会议来展示他们的科学肌肉。他们提出了你能想到的每一种机制，能想到的每一个组织，从胰脏到肌肉，再到肝脏，再到大脑，再到你的血液。

 

说胰岛素抵抗有一个原因是不恰当的。说胰岛素抵抗是一种复杂的代谢情况， 更准确。

 

然而，尽管如此，实验室环境中的研究人员使用一种简单的技术，却能轻易地在实验室动物体内诱导出胰岛素抵抗 。 尽管无休止的学术争论，有一件事是清楚的——如果你想在实验动物或人类身上诱导胰岛素抵抗，最有效和可重复的方法很简单:

 

胰岛素抵抗是由脂质超载(Lipid Overload or Fat Overload) 引起的，或者由高脂肪饮食引起的，或者是由于缺乏运动导致的脂肪“燃烧”不足所致。

　

　

 或者

　

　

 

胰岛素抵抗原因1:高脂肪饮食 (High Fat Diet)

访问地球上任何一个研究动物或人类胰岛素抵抗的实验室，你会注意到一种简单的技术，它以可重复的方式实现胰岛素抵抗——吃高脂肪的食物。而不是碳水化合物。

　

　

 

在一些研究中，研究人员使用高脂肪 （High Fat Diet ) 和高蔗糖(蔗糖)的饮食 (High Sucrose Diet)，以确保肌肉和肝脏都变得非常胰岛素抵抗。原因很简单:

 

摄入大量的膳食脂肪会导致肌肉和肝脏的脂质超载和胰岛素抵抗。蔗糖(白糖) (High Sucrose Diet) 也会增加肝脏的胰岛素抵抗。

　

　

 

我经常被问到是否有任何研究支持脂肪酸引起胰岛素抵抗的说法。有大量的研究证明了这一观点，而这一证据清楚地表明，过量的脂肪酸是导致肌肉和肝脏胰岛素抵抗的主要原因。一个简单的文献搜索揭示了如下的语句:

 

“长时间暴露于骨骼肌和肌细胞中，高水平的脂肪酸会导致严重的胰岛素抵抗(2,3)。在不同类型的脂肪酸中，饱和的长链脂肪酸，如棕榈酸和硬脂酸被证明是胰岛素抵抗的有效诱导因子(4,5)。我们(4,6 - 8)和其他(2,9-12)建议了几种机制来解释饱和脂肪酸是如何影响胰岛素作用的，如Randle循环，细胞内脂质衍生物的积累(二酰基甘油和神经酰胺)，氧化应激，基因转录的调节，炎症和线粒体功能障碍。在本综述中，我们讨论了支持这些机制参与饱和脂肪酸对胰岛素敏感性调节的证据，并提出在脂肪酸水平升高的条件下发现的线粒体功能障碍在胰岛素抵抗的发病机制中起着中心作用(13)。

　

　

　

 

饱和脂肪酸是胰岛素抵抗的最有影响力的影响因素。

饱和脂肪酸主要来源于动物，对肌肉和肝脏有直接的负面影响。

 

以下动物食物中含有高浓度的饱和脂肪酸:

动物肉(牛肉、鸡肉、猪肉、火鸡、鸭、鹿肉等)

奶牛、山羊和绵羊的奶制品(牛奶、黄油、酸奶油、奶油干酪、奶酪)

鱼(鳕鱼、鲱鱼、鲑鱼、沙丁鱼等)

此外，一些植物食物中含有高浓度的饱和脂肪，包括:

坚果和种子(巴西坚果、澳洲坚果、腰果、松子和芝麻)

干椰子肉

氢化植物油

 

饱和脂肪酸摄入对肌肉和肝脏的直接影响包括:

肌肉和肝脏的线粒体功能障碍；

在肌肉和肝脏中产生自由基；

肌肉和肝脏的细胞炎症；

 

当多余的脂肪堆积在肌肉和肝脏组织中时，葡萄糖进入这两种组织的能力就会大大受损。

 

在另一篇关于饱和脂肪酸对组织功能影响的论文中，作者指出:

“过度积累未氧化的长链脂肪酸会使脂肪组织的储存能力饱和，导致脂质‘溢出’到非脂肪组织，如肝脏、肌肉、心脏和胰脏胰岛。”在这种情况下，这样的异位脂质沉积会产生有害的影响。多余的脂质被驱动进入替代的非氧化途径，从而形成反应性脂质，促进新陈代谢相关的细胞功能紊乱(脂毒性)和程序性细胞死亡(脂细胞凋亡)(14)。

 

一些研究人员已经阐明了脂肪酸诱发低级别炎症的能力，这是一系列导致血管受损的一系列事件的初始步骤。

 

从上至下的观点来看，高脂肪饮食会按一下方式导致胰岛素抵抗:

尽管有证据表明过量的脂肪摄入会导致过多的脂肪储存，但通常情况下，碳水化合物被认为是导致胰岛素抵抗的罪魁祸首。

 

胰岛素抵抗原因# 2: 假的碳水化合物 （Fake Carbohydrates)

我已经广泛地谈论了真实和假碳水化合物的区别，并详细讨论了它们对你身体组织的影响。你可以在文章中了解到碳水化合物并不能杀死你:第一部分。

为了不让你浏览之前的文章，让我们再来看看真实的和虚假的碳水化合物的区别。

 

真正的碳水化合物是什么?

真正的碳水化合物主要来自水果和蔬菜，可以在它们的整个自然状态中食用，很少烹饪或加工。真正的碳水化合物主要存在于植物类食物中，并预先包装了大量的维生素、矿物质、抗氧化剂、纤维素和水。把真正的碳水化合物想象成你在森林中独自行走是发现的食物。

 

真正的碳水化合物具有不可估量的健康益处，而且是追求最佳的运动表现、运动恢复和防止脂质过载者所必需。

 

假的碳水化合物是什么?

假碳水化合物生活在包装、瓶子、罐子和盒子里。它们是经过加工、制造和改变的“精制”产品。假碳水化合物已经从原来的状态被修改，以使它们可以食用，并且经常让它们尝起来很甜。假碳水化合物包括谷物、谷物、面食、大米、面包和人工甜味剂。

 

　

　

食用假碳水化合物会导致灾难性的健康影响，包括(但不限于):

增加食欲和饮食过量(16)

肝脏脂肪合成增加(17,18)

多余的体重增加(16、17)

胰岛素抵抗、高血糖和糖尿病(17-19)

代谢综合征(18)

系统性炎症(19)

 

在过去的十年里，大量的证据已经开始揭示精制碳水化合物对心血管健康、糖尿病健康、肝脏健康和多余体重的影响。从这些条款中获得的声明包括:

 

“在胎儿、新生儿和婴儿发育的关键时期，高果糖暴露会影响终生的神经内分泌功能、食欲控制、进食行为、脂肪生成、脂肪分布和代谢系统。”这些变化最终有利于肥胖的长期发展和相关的代谢风险(16)。

 

“细粮消费高,尤其是白米,据报道与2型糖尿病的风险更高。这些结果表明,高消耗的大米和面条可能通过增加胰岛素抵抗导致高血糖症,这关系是独立于肥胖和系统性炎症(19)”。

 

胰岛素抵抗原因# 3: 缺少锻炼

运动无疑是提高胰岛素敏感性的最有效方法，被认为是降低糖尿病风险的黄金标准方法(20-27)。锻炼对肌肉组织的胰岛素抵抗有三个主要原因:

运动刺激肌肉组织燃烧储存的脂肪。

运动刺激肌肉组织接受血液中的葡萄糖。

运动允许肌肉在没有胰岛素的情况下接受葡萄糖。

　

　

　

 

把锻炼看成是增强肌肉组织吸收血液中葡萄糖的信号。强迫肌肉在短时间内收缩和拉长数千次，增加了脂肪燃烧的能力，同时也增加了储存更多葡萄糖的意愿。就胰岛素抵抗而言，这是双重打击。

 

运动在短期和长期都有作用，并导致肌肉组织对血液中葡萄糖的反应能力显著增强。

“一场运动可以通过一种胰岛素独立机制来增加骨骼肌葡萄糖摄取，这种机制可以绕过与这些条件相关的典型胰岛素信号缺陷。”然而，这种“胰岛素增敏”效应是短暂的，在48小时后就消失了。相反，重复的身体活动(即运动训练)会导致肥胖和胰岛素抵抗的个体在骨骼肌中持续增加胰岛素作用(28)。

　

　

 

我很高兴地看到，无论他们是否患有糖尿病，运动都被作为有胰岛素抵抗个体的治疗手段。在许多情况下，那些有糖尿病前期的人可以通过定期的锻炼计划来延缓糖尿病的转变，定期提高胰岛素的敏感性。

 

“因此，现在已经广泛承认，定期的体育锻炼能够有效地治疗有骨骼肌胰岛素抵抗的胰岛素抵抗患者。

　

　

 

带回家的消息

重要的是要认识到胰岛素抵抗会影响到每个人，即使是那些没有表现出高血糖症状的人。为了确保你保持胰岛素敏感性，不管你目前的健康状况(糖尿病或非糖尿病)，遵循以下三个步骤:

食用脂肪占热量不到15%热量的饮食。

减少或消除你对假碳水化合物的消耗。

保持每周进行3-4次增强心肺功能的有氧运动。

　

　

 

What Causes Insulin Resistance? Lipid Overload

Cyrus Khambatta

　

Over the past year I have interacted with hundreds of people with diabetes, and have come to learn one very important lesson that has changed my view of diabetes altogether. This realization came to me early on in my career as a nutrition and fitness coach for people with diabetes, and continues to hold true.

 

While insulin resistance is a condition that is most commonly associated with type 2 diabetes, an increasing body of evidence is now shedding light on the fact that insulin resistance is a common thread that underlies many health conditions previously unassociated with blood sugar, including (but not limited to) heart disease, diabetes, atherosclerosis, the metabolic syndrome, obesity and cancer.

 

What that means is simple: insulin resistance significantly increases your risk for the development of a collection of health conditions that can significantly reduce your quality of life and decrease your life expectancy.

 

Watch this video for a synopsis of the causes of insulin resistance:

 

 

What is insulin and why should you care?

Insulin is a hormone which is released by the pancreas in response to rising blood glucose. When you consume carbohydrates, the glucose that enters the bloodstream knocks on the door of the beta cells in the pancreas as a signal to make insulin.

 

Insulin serves as the key that unlocks the door to allow glucose to enter body tissues. Insulin tells your cells “Yoo hoo! Pick up this glucose. It’s all over the place.”

Without insulin, cells in the liver, muscle, and fat have a difficult time vacuuming up glucose from the blood. These tissues are capable to vacuuming up only a small percentage (5-10%) of the glucose in circulation without the help of insulin. When insulin is present, the amount of glucose that can be transported into tissues significantly increases, allowing tissues to be properly fed, and keeping blood glucose concentrations in the normal range. The system looks like this:

 

 

What is insulin resistance?

Insulin resistance is a condition in which multiple tissues in the human body become resistant to the effects of insulin. Simply stated, insulin resistance occurs when tissues become “dumb” to insulin.

 

As a result of insulin resistance, the pancreas is forced to secrete increasing amounts of insulin, resulting in a condition known as hyperinsulinemia.

Hyperinsulinemia is a dangerous condition for many tissues, simply because elevated insulin concentrations in the blood act as potent signals for cell growth. More insulin means more tissue growth. More tissue growth often results in increased fatness, increased cell replication rates and a significant increase in the risk for cancer. Many studies have now begun to uncover the link between insulin resistance and cancer, and one such study states the following:

 

"Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in which circulating insulin levels are frequently increased. Recent epidemiological and clinical evidence points to a link between insulin resistance and cancer. The mechanisms for this association are unknown, but hyperinsulinaemia (a hallmark of insulin resistance) and the increase in bioavailable insulin-like growth factor I (IGF-I) appear to have a role in tumor initiation and progression in insulin-resistant patients (1)."

How much do scientists know about insulin resistance?

There is a significant amount of confusion about what actually causes insulin resistance, and in my life as a type 1 diabetic as well as my career as a research scientist, I have come to realize that life-saving information about insulin resistance is poorly understood.

 

There exists a large wall between what the research world understands about insulin resistance and what the general public understands about insulin resistance. Unfortunately, excellent research does no good if the information is not put in the hands of those who need it. This is certainly the case with insulin resistance. The picture looks something like this:

 

 

This wall exists for a number of reasons, and is heavily influenced by economic forces that profit on lifelong health conditions like diabetes. You may have heard the phrase “there is no money in the cure.” This is a true statement, and this practice is what keeps life-saving information out of the hands of those who need it.

 

What causes insulin resistance?

Researchers debate the causal mechanisms of insulin resistance tirelessly, day after day, and travel thousands of miles to attend large conferences to flex their scientific muscles. They propose every mechanism you can imagine, and blame every tissue you can think of, from the pancreas to the muscle to the liver to the brain to your blood.

 

To say that insulin resistance has a single cause is a misnomer. To say that insulin resistance is a complex metabolic condition is much more accurate.

 

Despite this, however, researchers in the laboratory environment can induce insulin resistance in laboratory animals an in humans incredibly easily, using one simple technique. Regardless of the endless intellectual debate, one thing remains clear - if you want to induce insulin resistance in a laboratory animal or in a human, the most effective and repeatable way to do it is simple:

 

Insulin resistance is caused by lipid overload, resulting from either a high fat diet or insufficient fat “burning” through movement.

Insulin Resistance Cause #1: High Fat Diet

Visit almost any laboratory on the planet that studies insulin resistance in animals or in humans and you’ll notice one simple technique that achieves insulin resistance in a repeatable fashion – eating a diet high in fat. Not carbohydrates.

 

In some studies, researchers use a diet high in fat and high in sucrose (table sugar), to ensure that both the muscle and the liver become extremely insulin resistant. The reason for this is simple:

 

A high intake of dietary fat causes lipid overload and insulin resistance in the muscle and liver. Sucrose (white table sugar) also increases liver insulin resistance.

 

 

I am often asked whether there is any research to back up the claim that fatty acids cause insulin resistance. There is a considerable amount of research that justifies this notion, and this evidence clearly points to the fact that excess fatty acids are a potent cause of both muscular and liver insulin resistance. A simple literature search reveals statements like the following:

 

"Prolonged exposure of skeletal muscle and myocytes to high levels of fatty acids leads to severe insulin resistance(2,3). Among the different types of fatty acids, saturated long-chain fatty acids such as palmitic and stearic acids were demonstrated to be potent inducers of insulin resistance(4,5). Several mechanisms have been suggested by us(4,6–8) and others(2,9–12) to explain how saturated fatty acids impair insulin actions such as the Randle cycle, accumulation of intracellular lipid derivatives (diacylglycerol and ceramides), oxidative stress, modulation of gene transcription, inflammation and mitochondrial dysfunction. In the present review, we discuss evidence supporting the involvement of these mechanisms in the regulation of insulin sensitivity by saturated fatty acids and propose the mitochondrial dysfunction found in conditions of elevated fatty acid levels has a central role in the pathogenesis of insulin resistance(13)."

Saturated fatty acids are the most potent influencers of insulin resistance

Saturated fatty acids are derived mainly from animal sources, and have direct negative effects on the muscle and liver.

 

High concentrations of saturated fatty acids are found in the following animal foods:

 

Animal meat (beef, chicken, pork, turkey, duck, venison etc.),

Dairy products from cows, goats and sheep (milk, butter, sour cream, cream cheese, cheese)

Fish (cod, herring, salmon, sardines etc.)

In addition, high concentrations of saturated fats are found in some plant foods, including:

 

Nuts and seeds (brazil nuts, macadamia nuts, cashew nuts, pine nuts and sesame seeds)

Dried coconut meat

Hydrogenated vegetable oils

These direct effects of saturated fatty acid intake on muscle and liver include include:

 

Mitochondrial dysfunction in the muscle and liver

The production of free radicals in the muscle and liver

Cellular inflammation in the muscle and liver

When excess fat accumulates it the muscle and liver tissue, the ability of glucose to enter both tissues is significantly compromised. In another paper written about the effect of saturated fatty acids on tissue function, the authors state the following:

 

"An overaccumulation of unoxidized long-chain fatty acids can saturate the storage capacity of adipose tissue, resulting in a lipid ‘spill over’ to non-adipose tissues, such as the liver, muscle, heart, and pancreatic-islets. Under these circumstances, such ectopic lipid deposition can have deleterious effects. The excess lipids are driven into alternative non-oxidative pathways, which result in the formation of reactive lipid moieties that promote metabolically relevant cellular dysfunction (lipotoxicity) and programmed cell-death (lipoapoptosis)(14)."

Several investigators have shed light on the ability of fatty acids to induce low-grade inflammation, which acts as an initial step in a series of events leading to damaged blood vessels, liver disease, heart disease and hypertension:

 

"Elevated free fatty acid levels (due to obesity or to high-fat feeding) cause insulin resistance in skeletal muscle and liver, which contributes to the development of type 2 diabetes mellitus (T2DM), and produce low-grade inflammation, which contributes to the development of atherosclerotic vascular diseases and NAFLD (non-alcoholic fatty liver disease)(15)."

From a top-down view, a high fat diet induces insulin resistance in the following way:

 

 

Too often, the blame is placed on carbohydrates as the cause of insulin resistance despite the fact that the evidence clearly supports that excessive fat consumption causes excessive fat storage.

 

Insulin Resistance Cause #2:

FAKE Carbohydrates

I’ve talked extensively about the difference between REAL and FAKE carbohydrates, and gone into detail about the effects they have on tissues throughout your body. You can read about them in the article Carbohydrates are NOT Killing You: Part 1.

 

To save you from having to scroll through previous articles, let’s walk through the difference between REAL and FAKE carbohydrates once again.

 

What are REAL carbohydrates?

REAL carbohydrates come from mainly fruits and vegetables, and can be eaten in their whole, natural state with minimal cooking or processing. REAL carbohydrates are found mainly in plant foods, and come pre-packaged with a host of vitamins, minerals, antioxidants, fiber and water. Think of REAL carbohydrates as the types of foods that you would find if you were walking in the woods by yourself.

 

 

REAL carbohydrates have untold health benefits, and are absolutely required for optimal athletic performance, athletic recovery and preventing against lipid overload.

 

What are FAKE carbohydrates?

FAKE carbohydrates live in packages, bottles, cans and boxes. They are “refined” products that have been processed, manufactured and changed from their original and whole state. FAKE carbohydrates have been modified from their original state in order to make them edible and often times to make them taste sweet. FAKE carbohydrates include grains, cereals, pastas, rice, bread products and artificial sweeteners.

 

 

Consumption of FAKE carbohydrates can lead to disastrous health effects, including (but not limited to):

 

Increased appetite and overeating(16)

Increased fat synthesis in the liver(17,18)

Unwanted weight gain(16,17)

Insulin resistance, high blood sugar and diabetes(17–19)

The metabolic syndrome(18)

Systemic inflammation(19)

In the past decade, a large body of evidence has begun to uncover the potent effects of refined carbohydrates on decreased cardiovascular health, diabetes health, liver health and unwanted weight gain. Statements taken from these articles include:

 

"High fructose exposure during critical periods of development of the fetus, neonate and infant can act as an obesogen by affecting lifelong neuroendocrine function, appetite control, feeding behaviour, adipogenesis, fat distribution and metabolic systems. These changes ultimately favour the long-term development of obesity and associated metabolic risk (16)."

 

"High consumption of refined grains, particularly white rice, has been reported to be associated with a higher risk of type 2 diabetes…These results suggest that high consumption of rice and noodles may contribute to hyperglycaemia through greater insulin resistance and that this relationship is independent of adiposity and systemic inflammation (19)."

Insulin Resistance Cause #3:

Insufficient Exercise

Exercise is without doubt the most effective method of increasing insulin sensitivity, and is considered the gold-standard method of decreasing diabetes risk(20–27). There are three main reasons why exercise benefits insulin resistance in muscle tissue:

 

Exercise stimulates the muscle tissue to burn stored fat

Exercise stimulates the muscle tissue to accept glucose from the blood

Exercise allows the muscle to accept glucose without the help of insulin

Think of exercise as being the signal that increases the appetite of your muscle tissue to accept incoming glucose in the blood. Forcing the muscle to contract and elongate thousands of times in a short period of time increases it’s fat burning capabilities and also increases its willingness to store more glucose. As far as insulin resistance is concerned, this is a double whammy.

 

Exercise acts in both the short term and the long term, and leads to significant increases in the ability of the muscle tissue to respond to glucose in the blood.

 

"A single bout of exercise increases skeletal muscle glucose uptake via an insulin-independent mechanism that bypasses the typical insulin signalling defects associated with these conditions. However, this ‘insulin sensitizing’ effect is short-lived and disappears after ∼48 h. In contrast, repeated physical activity (i.e. exercise training) results in a persistent increase in insulin action in skeletal muscle from obese and insulin-resistant individuals (28)."

I am happy to see that exercise is now being prescribed as a treatment for insulin resistant individuals, regardless of whether they have diabetes or not. In many cases, those with prediabetes can stave off the transition to diabetes by adopting a regular exercise regimen to increase insulin sensitivity regularly.

 

"Accordingly, it is now well accepted that regular physical exercise offers an effective therapeutic intervention to improve insulin action in skeletal muscle in insulin-resistant individuals (29)."

Take Home Message

It is important to recognize that insulin resistance affects everyone, even those who show no symptoms of high blood sugar. In order to ensure that you remain insulin sensitive, regardless of your current health status (diabetic or non-diabetic), follow these three steps:

 

Consume a diet containing less than 15% of calories from fat

Minimize or eliminate your consumption of FAKE carbohydrates

Maintain a consistent exercise regimen with 3-4 sessions of cardiovascular exercise per week

　

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