Diabetes Is Not Just a Sugar Problem: A Deep Dive into Insulin Resistance

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Chapter 1. Introduction: Insulin, the Master Key to Blood Sugar Control

In the modern health landscape, diabetes has become more than just a disease; it's a global phenomenon. Many people understand diabetes through a simplistic formula: excessive consumption of sugar or carbohydrates. However, this is merely the final outcome of a complex metabolic process and fails to explain the core of the problem. Beneath the surface of Type 2 diabetes lies a massive, underlying systemic collapse that develops silently over many years: 'Insulin Resistance.' This article aims to move beyond the stereotype of 'sugar = diabetes' and provide an in-depth analysis of why insulin resistance is the starting point and central link in modern metabolic diseases.

1.1. Glucose: Our Body's Energy Currency

For every cell in our body to function, it needs energy, and the most fundamental energy source is glucose.1 The brain, in particular, relies almost exclusively on glucose to maintain its functions. The food we eat, especially carbohydrates like rice and bread, is broken down into glucose through digestion and absorbed into the bloodstream. The blood then transports this glucose to every cell in our body. The concentration of glucose in the blood is called 'blood sugar.' A healthy body has a sophisticated system to maintain this blood sugar within a very narrow, stable range.

1.2. The Role of Insulin: From Gatekeeper to Conductor

At the heart of the blood sugar control system is insulin, a hormone secreted by the beta cells of the pancreas.2 When blood sugar rises after a meal, the pancreas detects this and releases insulin. Insulin's most well-known role is to open the 'door' for glucose in the blood to enter the cells.2 Glucose enters muscle cells to be used as immediate energy or is stored in the liver and muscles in the form of glycogen.5 Through this process, the blood glucose level returns to a stable state. Insulin is critically important as it is virtually the only hormone in our body that lowers blood sugar.5

However, insulin's role is not limited to being a simple 'gatekeeper' for glucose. It is the 'maestro' that orchestrates our body's entire energy metabolism. Beyond glucose metabolism, it promotes the absorption of fatty acids by fat cells for storage as triglycerides and inhibits the breakdown of already stored fat. It also facilitates the entry of amino acids into cells to promote protein synthesis, overseeing the overall anabolic process—that is, storing energy and building tissues.5 Thus, insulin is a key signal that enables our body to use and store energy efficiently.

1.3. What Is Insulin Resistance? Understanding the Concept Through an Analogy

Insulin resistance is a condition where the body's cells (especially in the liver, muscles, and fat) do not respond properly to the signal of insulin, even when normal levels are present in the blood.6

To understand this easily, we can use the 'crowded subway' analogy.11 Imagine the cell is a 'subway car,' the glucose in the blood is the 'passengers,' and insulin is the 'pusher' who helps passengers get on board. Normally, with the help of the pusher (insulin), passengers (glucose) board the subway (cell) smoothly. But what if the subway car is already packed with passengers (fat) due to excessive energy intake? No matter how many pushers come and push, there is no more room. This state is insulin resistance. The cell, in a state of energy surplus, refuses to accept more glucose.

Another analogy is a 'rusty lock.' To open the door to the house (the cell), you need a key (insulin). But if the lock becomes rusty and stiff, the door won't open easily even when you turn the key. To open the door, our body starts producing more and stronger keys (insulin). This leads to an abnormally high concentration of insulin in the blood, a condition called 'hyperinsulinemia'.12 For the first few years, or even decades, blood sugar can be maintained within a normal range thanks to this compensatory action of the pancreas over-secreting insulin. Because there are no symptoms, most people are unaware of this silent war raging inside their bodies. This is why insulin resistance is called a 'silent disease'.13

1.4. Beyond Sugar: Why Insulin Resistance Is the Core of Modern Metabolic Disease

In conclusion, Type 2 diabetes is not a disease that suddenly appears from eating too much sugar. It is a phenomenon that manifests only when the fundamental systemic failure of insulin resistance, which has progressed over many years, reaches a tipping point where the exhausted pancreas can no longer compensate.13

More importantly, insulin resistance is not just a stepping stone to diabetes. It is identified as the common root and starting point for numerous modern chronic diseases, including metabolic syndrome, hypertension, dyslipidemia, cardiovascular disease, non-alcoholic fatty liver disease, polycystic ovary syndrome, and more recently, some cancers and dementia.13 Therefore, understanding insulin resistance is equivalent to grasping the core principle that runs through our entire metabolic health, beyond individual diseases. This post will delve deeply into this core principle.

Chapter 2. The Onset of Insulin Resistance: The Beginning of an Invisible Danger

Insulin resistance does not arise from a single cause but develops gradually over many years through a complex interplay of genetic predisposition and various lifestyle factors such as diet, physical activity, stress, and sleep. It is particularly noteworthy that these factors do not act independently but amplify each other, forming a 'Metabolic Vicious Cycle.'

2.1. The Main Culprit, Visceral Fat: Not Just an Energy Storehouse but an Endocrine Organ

The most potent and direct factor causing insulin resistance is obesity, especially the accumulation of visceral fat, which is the fat stored between the abdominal organs.15 In the past, adipose tissue was considered a passive storage depot for excess energy. However, modern medicine has revealed that visceral fat is a large 'endocrine organ' that actively secretes various bioactive substances.18

The problem is that the substances secreted by visceral fat have harmful effects on our body. Enlarged visceral fat cells release inflammatory cytokines such as tumor necrosis factor-alpha () and interleukin-6 (), as well as large amounts of Free Fatty Acids (FFA), into the bloodstream.18 These substances travel directly to the liver and muscles, physically interfering with the normal insulin signaling process within the cells. This promotes a state of chronic low-grade inflammation, which is a key mechanism for inducing and exacerbating insulin resistance.20

2.2. The Betrayal of Diet: Excessive Refined Carbohydrates and Chronic Hyperinsulinemia

Frequent consumption of refined carbohydrates such as sugar, high-fructose corn syrup, white flour, and white rice is another major cause of insulin resistance.9 These foods are digested and absorbed very quickly, causing a rapid spike in post-meal blood sugar (blood sugar spike).1 To handle this emergency, our body rapidly secretes a large amount of insulin from the pancreas.24

When this 'high blood sugar-high insulin' rollercoaster is repeated chronically, the cell's insulin receptors become desensitized to the constant overstimulation.6 This is similar to how one becomes accustomed to noise in a loud construction site. Furthermore, the state of chronic hyperinsulinemia itself acts as a powerful anabolic signal, converting excess glucose into fat and storing it in the liver and abdomen, promoting inflammatory responses, and increasing sodium reabsorption in the kidneys, which raises blood pressure. This creates a vicious cycle that worsens insulin resistance.23

2.3. The Silent Disruptors: Chronic Inflammation, Stress, and Sleep Deprivation

Beyond visible factors like diet and weight, invisible lifestyle factors have a profound impact on the development of insulin resistance.

• Chronic Low-Grade Inflammation: In addition to visceral fat, chronic inflammation from various sources such as gut dysbiosis, latent infections, and exposure to environmental toxins is itself a core driver of insulin resistance. Inflammatory signals directly damage the insulin signaling pathway, reducing the system's efficiency.13

• Stress and Sleep Deprivation: Chronic stress and lack of sleep, inseparable from modern life, are powerful disruptors that worsen insulin resistance. In stressful situations or during sleep deprivation, our body releases the stress hormone cortisol for the 'fight-or-flight' response.25 Cortisol directly raises blood sugar by promoting glucose production in the liver and interferes with insulin's action, causing resistance. Moreover, lack of sleep decreases the secretion of leptin, a hormone that suppresses appetite, while increasing the secretion of ghrelin, which stimulates appetite, leading to cravings for high-calorie foods.25 Research has shown that not only short sleep (less than 6 hours) but also excessively long sleep (more than 8 hours) can increase the risk of insulin resistance, emphasizing the importance of both sleep quantity and quality.27

2.4. The Interplay of Genetics and Environment

Genetic predisposition clearly plays a role in the development of insulin resistance. Individuals with a family history of Type 2 diabetes have a higher risk of developing it.9 However, genes are just the 'loaded gun'; environmental factors pull the trigger. Insulin resistance manifests when lifestyle factors such as a Westernized high-calorie diet, lack of physical activity, and chronic stress combine with genetic vulnerability.29

The interaction of these causes explains why insulin resistance tends to worsen once it begins. For example, visceral fat causes inflammation, which worsens insulin resistance, and worsened insulin resistance promotes further fat accumulation, increasing visceral fat. This forms a vicious cycle that gradually breaks down the metabolic system over time. Therefore, managing insulin resistance requires an integrated approach that simultaneously breaks multiple links in this cycle.

Chapter 3. Malfunction at the Cellular Level: The Molecular Biology of Insulin Resistance

Having understood the macroscopic causes of insulin resistance, it is now necessary to delve into the cell to see what malfunctions are occurring at the molecular level. Understanding how the insulin signal is transmitted and how this sophisticated system is disrupted in a state of insulin resistance is the key to accessing the core of the problem.

3.1. The Insulin Signaling Pathway: The Response Process of a Normal Cell

The process by which insulin regulates blood sugar is a sophisticated chain reaction of signal transduction within the cell. This process can be broadly divided into three stages:

1. Receptor Binding and Activation: An insulin molecule in the blood binds to the alpha () subunit of the insulin receptor on the cell surface. This binding is like a key fitting into a lock, causing a structural change in the receptor. This change activates the tyrosine kinase enzyme of the beta () subunit, which is located inside the cell membrane.30

2. Signal Amplification (Phosphorylation of IRS-1): The activated tyrosine kinase phosphorylates itself and surrounding proteins. One of the most important targets is the 'Insulin Receptor Substrate-1 (IRS-1)'. IRS-1 has multiple tyrosine residues, and the insulin receptor phosphorylates these sites, acting as a 'docking station' to transmit and amplify the signal into the cell.33

3. Activation of the PI3K-Akt Pathway: Tyrosine-phosphorylated IRS-1 attracts and activates an enzyme called PI3K (Phosphatidylinositol 3-kinase). Activated PI3K phosphorylates specific phospholipids in the cell membrane to create secondary signaling molecules, which in turn activate a key regulatory protein called Akt (or Protein Kinase B, PKB). This 'PI3K-Akt pathway' is the most important signaling pathway that mediates insulin's main metabolic actions, such as glucose uptake, glycogen synthesis, and protein synthesis.35

3.2. Disruption of Signal Transduction: How Inflammation and Free Fatty Acids Interfere

The core of insulin resistance is the blockage of the PI3K-Akt pathway described above. This disruption of signal transduction is primarily caused by chronic inflammation and excessive free fatty acids.

• The Attack of Inflammation and Lipotoxicity: Inflammatory cytokines (, etc.) secreted from visceral fat activate stress-inflammatory kinases like JNK and IKKβ within the cell.20 Simultaneously, excessive free fatty acids are converted into and accumulate as lipid metabolites such as DAG (Diacylglycerol) and Ceramide within the cell (lipotoxicity). DAG, in particular, activates another type of kinase called PKC (Protein Kinase C).36

• Phosphorylation at the Wrong Site: The crux of the problem is that these activated inflammatory and stress kinases (JNK, IKKβ, PKC) phosphorylate the serine/threonine residues of IRS-1, not the normal tyrosine residues.36 This phosphorylation at the 'wrong site' alters the three-dimensional structure of the IRS-1 protein, physically preventing its normal binding with the insulin receptor or PI3K. As a result, even if insulin binds to the receptor, the signal is not properly transmitted to the PI3K-Akt pathway, leading to a 'disruption of signal transduction.' This is the core molecular mechanism of insulin resistance.

3.3. Failure of Glucose Transport: The Role and Dysfunction of GLUT4

One of the final goals of the PI3K-Akt pathway is to transport glucose from the blood into the cell. The 'Glucose Transporter type 4 (GLUT4)' plays a crucial role in this process.

• Normal Function: Normally, GLUT4 is stored inside small vesicles within the cell. When Akt is activated by the insulin signal, this signal commands the vesicles containing GLUT4 to move to the cell membrane.38 Once at the cell membrane, GLUT4 fuses with the membrane to form a 'channel' for glucose to pass through, allowing glucose from the blood to flood into the cell.40

• Dysfunction: In a state of insulin resistance, because the PI3K-Akt pathway is blocked, the signal to move GLUT4 to the cell membrane is not properly transmitted. As a result, despite having sufficient GLUT4 inside the cell, very few glucose channels open on the cell membrane.41 Outside the closed door of the cell, glucose has nowhere to go and continues to accumulate in the blood, leading to a chronic state of hyperglycemia.

3.4. Selective Insulin Resistance: The Key to Unlocking the Paradox of Disease

Here, the most cunning and important feature of insulin resistance is revealed. The insulin signal is not a single pathway but branches into two main routes. One is the PI3K-Akt pathway, which is responsible for metabolic regulation as described earlier, and the other is the Ras/MAPK pathway, which is involved in cell growth, proliferation, and inflammatory responses.43

Insulin resistance does not affect these two pathways equally. Inflammation and lipotoxicity selectively block the PI3K-Akt pathway. In contrast, the Ras/MAPK pathway remains relatively unaffected or even activated.

This is the concept of 'Selective Insulin Resistance,' and it provides a key insight into why insulin resistance causes various diseases. In a state of hyperinsulinemia, our body pumps out excessive amounts of insulin to stimulate the desensitized PI3K-Akt pathway. This excess insulin has little effect on the blocked metabolic pathway but continuously overstimulates the still-responsive Ras/MAPK pathway.45

As a result, a person with insulin resistance faces a paradoxical situation:

• Glucose metabolism is impaired, and blood sugar is not controlled (PI3K-Akt pathway resistance).

• Simultaneously, excessive insulin stimulation can lead to the proliferation of vascular smooth muscle cells, promoting atherosclerosis; increased secretion of vasoconstrictors (endothelin-1), raising blood pressure; worsening of inflammatory responses; and promotion of the growth of certain cancer cells (Ras/MAPK pathway overactivation).45

Thus, insulin resistance is not just a metabolic disorder where blood sugar rises, but a complex pathophysiology that is the fundamental cause of systemic vascular and proliferative diseases.

Chapter 4. One Root, Many Branches: Systemic Diseases Caused by Insulin Resistance

Insulin resistance is not a single disease but acts as a 'Common Pathophysiological Hub' underlying most of the major modern non-communicable diseases (NCDs). Understanding how various diseases such as metabolic syndrome, cardiovascular disease, non-alcoholic fatty liver disease, and polycystic ovary syndrome branch out from the single root of insulin resistance is essential for their integrated prevention and management.

4.1. Metabolic Syndrome: Five Risk Signals Threatening Modern Health

Metabolic Syndrome is a condition based on insulin resistance where several diseases, each a risk factor for cardiovascular disease on its own, appear together in one individual.47 These five components are not separate issues but different expressions of a single disease group derived from the common root of insulin resistance.48 The diagnostic criteria for metabolic syndrome are presented by several organizations, but the most widely used are as follows 51:

Component	NCEP-ATP III Criteria (≥3 criteria met)	IDF Criteria (Central Obesity required + ≥2 criteria met)
Abdominal Obesity (Waist Circumference)	Men ≥90 cm, Women ≥85 cm (Asian standards)	Men ≥90 cm, Women ≥80 cm (Asian standards)
High Triglycerides	≥ 150 mg/dL or on medication	≥ 150 mg/dL or on medication
Low HDL Cholesterol	Men < 40 mg/dL, Women < 50 mg/dL or on medication	Men < 40 mg/dL, Women < 50 mg/dL or on medication
High Blood Pressure	≥ 130/85 mmHg or on medication	≥ 130/85 mmHg or on medication
High Fasting Glucose	≥ 100 mg/dL or on medication	≥ 100 mg/dL or diagnosed with Type 2 Diabetes

A diagnosis of metabolic syndrome increases the risk of developing cardiovascular disease by 1.5 to 3 times and Type 2 diabetes by 3 to 5 times, even in individuals without diabetes, compared to the general population.14

4.2. Cardiovascular Disease: The Invisible Hand Accelerating Atherosclerosis

Insulin resistance and hyperinsulinemia promote atherosclerosis and increase the risk of cardiovascular disease through various pathways.

• Atherogenic Dyslipidemia: Insulin resistance causes a characteristic lipid abnormality. Increased synthesis of very-low-density lipoprotein (VLDL) in the liver leads to high blood triglyceride levels (hypertriglyceridemia), while levels of high-density lipoprotein (HDL, good cholesterol), which acts as a vascular scavenger, decrease. Furthermore, low-density lipoprotein (LDL, bad cholesterol) particles become smaller and denser (small dense LDL), making them more likely to penetrate the arterial wall and oxidize, forming atherosclerotic plaques.12

• Endothelial Dysfunction: Due to 'selective insulin resistance,' the production of nitric oxide (NO), which relaxes blood vessels, decreases in the endothelial cells lining the blood vessels, while the production of endothelin-1 (ET-1), which constricts them, increases. This reduces the elasticity and impairs the function of the blood vessels.45

• Promotion of Hypertension and Thrombosis: Hyperinsulinemia directly raises blood pressure by promoting the reabsorption of sodium and water in the kidneys, increasing fluid volume.54 It also increases the secretion of substances (like PAI-1) that activate blood clotting factors and inhibit the process of dissolving clots, making it easier for blood clots to form within the vessels.54

4.3. Non-alcoholic Fatty Liver Disease (NAFLD): The Silent Threat Accumulating in the Liver

Non-alcoholic fatty liver disease (NAFLD) is so closely related to insulin resistance that it is often called its 'hepatic manifestation.' In a state of insulin resistance, fat breakdown in adipose tissue is not suppressed, leading to high levels of free fatty acids in the blood. These excess fatty acids pour into the liver through the portal vein.36 The liver, also in a state of insulin resistance, continues to release glucose into the blood (worsening hyperglycemia) while simultaneously converting the incoming free fatty acids into triglycerides and storing them in liver cells. This is the beginning of simple fatty liver, and when oxidative stress and inflammation are added, it can progress to hepatitis, cirrhosis, and even liver cancer.9

4.4. Polycystic Ovary Syndrome (PCOS) and Hormonal Imbalance

Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, and insulin resistance is deeply embedded in its core pathophysiology.57 Hyperinsulinemia directly stimulates the ovaries to excessively produce androgens (male hormones) like testosterone. At the same time, it suppresses the production of sex hormone-binding globulin (SHBG) in the liver, further increasing the concentration of active free androgens in the blood.59 This hormonal imbalance disrupts the normal ovulatory function of the ovaries, leading to chronic anovulation, irregular or absent periods, and clinical symptoms such as hirsutism, adult acne, and male-pattern baldness, becoming a major cause of infertility.21

4.5. Cognitive Decline: The Potential Link to Depression and Dementia

The effects of insulin resistance are not limited to metabolic organs. Recent studies suggest that insulin resistance can also have serious effects on brain function. The brain is one of the important target organs for insulin, and abnormalities in insulin signaling in the brain are closely related to neuroinflammation, increased oxidative stress, and impaired energy metabolism in nerve cells.62 Large-scale cohort studies have shown that groups with high insulin resistance indicators have a significantly increased risk of developing depression compared to those with low indicators.63 There is also strong accumulating evidence that, in the long term, insulin resistance can increase the risk of cognitive decline and neurodegenerative diseases such as Alzheimer's disease, leading some to call Alzheimer's 'Type 3 diabetes.'

Thus, diseases treated by various medical specialties actually share a common denominator: insulin resistance. This strongly suggests that diseases should not be viewed solely as problems of individual organs but approached from an integrated perspective of a systemic metabolic imbalance.

Chapter 5. Restoring Metabolic Health: An Integrated Approach to Managing Insulin Resistance

While insulin resistance is the result of lifestyle habits formed over many years, it is not a hopeless condition. Through an integrated, evidence-based approach, it is possible to restore insulin sensitivity and regain metabolic balance. The key is not a 'restrictive' approach that forbids certain foods or forces strenuous exercise, but an 'environment-shaping' approach that continuously sends 'safety signals' to our body, encouraging it to restore itself to a normal state.

5.1. Diet Reconstruction: What, How, and When to Eat

Dietary management is the cornerstone of improving insulin resistance. The goal is to avoid sharp spikes in blood sugar and insulin levels while reducing inflammation and normalizing cellular function.

• Controlling Carbohydrate Quality and Quantity: The most important principle is to minimize the intake of refined carbohydrates (sugar, high-fructose corn syrup, white flour, white rice) and processed foods that cause rapid blood sugar spikes.9 Instead, the diet should be centered on whole grains (brown rice, oats, quinoa), legumes, and non-starchy vegetables (green leafy vegetables, broccoli), which are digested and absorbed slowly and are rich in dietary fiber. This helps to moderate the rise in blood sugar and reduce the burden on the pancreas.67

• Anti-Inflammatory Diet and Healthy Fats: Since chronic inflammation is a key driver of insulin resistance, it is important to actively consume foods with anti-inflammatory effects. Fatty fish rich in omega-3 fatty acids (salmon, mackerel), flaxseeds, walnuts, and foods rich in monounsaturated fats like olive oil, avocados, and various nuts help reduce inflammation and improve insulin sensitivity.72

• Sufficient Protein and Dietary Fiber: Quality protein (fish, chicken breast, tofu, legumes) and dietary fiber increase satiety, naturally helping to control total calorie intake, and slow the absorption of carbohydrates, stabilizing the blood sugar response. Eating vegetables or protein first before carbohydrates can also be effective in mitigating post-meal blood sugar spikes.64

• Foods that Improve Insulin Sensitivity: Some studies show that certain foods can have a positive impact on improving insulin sensitivity. Examples include catechins in green tea, cinnamon, anthocyanins in blueberries, and fermented foods like cheonggukjang (a Korean fermented soybean paste).75

5.2. Exercise Prescription: Making Muscles the Best Blood Sugar Management Organ

Exercise is one of the most effective ways to improve insulin resistance. This is because muscle is the key tissue that consumes and stores the most glucose in our body.77

• The Importance of Muscle: The more muscle mass you have, the larger the 'storage' for glucose, which is absolutely advantageous for blood sugar control. Building muscle through exercise is the surest investment in increasing insulin efficiency.78

• The Dual Effect of Exercise: Exercise regulates blood sugar through two pathways. First, it directly improves insulin sensitivity in the long term. Second, muscle contraction itself allows GLUT4 to move to the cell membrane and absorb glucose from the blood without the help of insulin.79 This means that blood sugar can be effectively lowered even when insulin function is impaired.

• Synergy of Aerobic and Resistance Exercise: Aerobic exercises like brisk walking, jogging, and cycling are effective for improving cardiovascular health and burning visceral fat. Resistance exercises like squats, lunges, and weight training fundamentally improve basal metabolic rate and glucose processing capacity by increasing muscle mass. The synergistic effect is greatest when these two types of exercise are combined.78 In particular, engaging in low-intensity physical activity, such as a light walk, 30 minutes to an hour after a meal is a very effective strategy to prevent post-meal blood sugar spikes.68

5.3. Lifestyle Correction: The Science of Sleep and Stress Management

Just as important as diet and exercise are sleep and stress management. They directly affect insulin sensitivity through hormonal balance.

• Ensuring Quality Sleep: Getting 7-8 hours of regular, deep sleep each night is essential for stabilizing the stress hormone cortisol and systemic inflammation levels, and for balancing appetite-regulating hormones (leptin, ghrelin).83 It is important to establish a habit of going to bed and waking up at a consistent time.

• Stress Management: Chronic stress continuously worsens insulin resistance through cortisol. It is necessary to find stress-relief methods that work for you, such as meditation, deep breathing, yoga, hobbies, or walks in nature, and integrate them into your daily life.9

• Quit Smoking and Limit Alcohol: Smoking itself causes oxidative stress and inflammation, and excessive alcohol consumption places a direct burden on the pancreas and liver, worsening insulin resistance.83

5.4. Medical Intervention and Adjunctive Therapies

While lifestyle improvement is fundamental, medical assistance can be combined if necessary.

• Medical Treatment: If blood sugar control is insufficient with lifestyle changes alone, or if specific conditions like polycystic ovary syndrome are present, a doctor may prescribe medications such as Metformin. Metformin works by suppressing glucose production in the liver and improving insulin sensitivity in peripheral tissues.86

• Nutritional Supplements: Some studies suggest that certain nutrients can provide ancillary help in improving insulin sensitivity. Representative examples include berberine, chromium, magnesium, coenzyme Q10, and omega-3 fatty acids, which can be considered as supplementary measures. However, before taking any nutritional supplements, it is essential to consult with a healthcare professional to determine the appropriate type and dosage for your individual condition.86

In conclusion, overcoming insulin resistance is not about a short-term diet or exercise program, but a shift to a way of life that prioritizes metabolic health. It is a holistic process of removing the chronic threat signals imposed on our body and creating a healthy environment where cells can once again listen to the signal of insulin. Through these steady efforts, we can prevent diabetes and free ourselves from the risk of numerous chronic diseases to regain health in its truest sense.

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21. 인슐린 저항성의 증상은? 매거진 - 닥터지노https://drjino.com/article/%EB%A7%A4%EA%B1%B0%EC%A7%84/12/5158/

22. 인슐린 저항성만으로도 혈전 생성? 의사들이 알려주지 않는 진실 - YouTubehttps://www.youtube.com/watch?v=1UxQsB-_W7Y

23. 심혈관질환 주범은 인슐린 저항성…“유연한 키토제닉 식단으로 잡아야” - 하이닥https://news.hidoc.co.kr/news/articleView.html?idxno=47456

24. 인슐린 저항성은 무엇이고 당뇨병은 왜 생길까 - (2011.11.5_390회 방송)_입체분석 3대 영양소의 진실 (1) - 달콤한 유혹, 탄수화물 - YouTubehttps://www.youtube.com/watch?v=wQz57nE3JLY

25. 당뇨병 부르는 인슐린 저항성, 잠 못 자도 높아져…올바른 수면 습관은 - ::고혈압 당뇨 및 만성질환관리 전문 현내과의원:::http://hyunmed.com/Module/News/News.asp?KEY=&MODE=V&KEYWORD=&PAGESIZE=10&PAGE=99&SRNO=33156

26. 당뇨병 그리고 불면 매거진 - 카카오헬스케어https://pastahealth.com/article/%EB%A7%A4%EA%B1%B0%EC%A7%84/8/211/

27. 비당뇨병 한국 성인의 수면시간과 인슐린 저항성의 관련성: 국민건강영양조사, 2019–2020 - Korean Journal of Family Practicehttps://www.kjfp.or.kr/journal/download_pdf.php?doi=10.21215/kjfp.2022.12.5.367

28. 수면장애와 당뇨병https://synapse.koreamed.org/func/download.php?path=L2hvbWUvdmlydHVhbC9rYW1qZS9zeW5hcHNlL3VwbG9hZC9TeW5hcHNlWE1MLzAxNzhqa2QvcGRmL2prZC0yMDIyLTIzLTMtMTg1LnBkZg==&filename=amtkLTIwMjItMjMtMy0xODUucGRm

29. 당뇨병 [diabetes mellitus] | 의학정보 | 건강정보 - 서울대학교병원https://www.snuh.org/health/nMedInfo/nView.do?category=DIS&medid=AA000260

30. 인슐린 신호전달계https://www.e-dmj.org/upload/pdf/dmj-29-5-383.pdf

31. 간에서의 당대사조절효소 유전자와 인슐린 신호전달https://www.e-dmj.org/upload/pdf/dmj-23-1-1.pdf

32. 인슐린 신호전달경로https://www.e-dmj.org/upload/pdf/dmj-17-4-337.pdf

33. 단백질 분해 조절을 통한 인슐린 신호전달의 조절 - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/1008jkse/jkse-20-434.pdf

34. Tyrosine kinase 수용체에 결합하는 호르몬의 작용기전 - 인슐린을 모델로 한 최신 이해-https://e-enm.org/upload/pdf/44501646.pdf

35. 제2형 당뇨병(Type II Diabetes Mellitus) (1) - 약학정보원https://common.health.kr/shared/healthkr/pharmreview/%EC%A0%9C2%ED%98%95%20%EB%8B%B9%EB%87%A8%EB%B3%91(Type%20II%20Diabetes%20Mellitus)%20(1).pdf

36. 인슐린저항성과 비알코올성 지방간질환https://www.e-cmh.org/upload/pdf/27402125.pdf

37. 인슐린 저항성: 메커니즘에서 치료 전략까지 - 당뇨신문https://www.dangnyoshinmun.co.kr/news/article.html?no=23783

38. ko.wikipedia.orghttps://ko.wikipedia.org/wiki/GLUT4#:~:text=%EC%A0%84%EB%8B%AC%20%EA%B2%BD%EB%A1%9C%EA%B0%80%20%EC%99%84%EB%A3%8C%EB%90%98%EB%A9%B4,%EC%84%B8%ED%8F%AC%20%EB%B0%98%EC%9D%91%EC%9D%84%20%EC%9C%A0%EB%B0%9C%ED%95%9C%EB%8B%A4.

39. 인슐린에 의한 GLUT4 전위과정에서 Rab Protein 및 Gh Protein의 역할에 관한 연구 - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/1201emj/emj-21-291.pdf

40. GLUT4 - 위키백과, 우리 모두의 백과사전https://ko.wikipedia.org/wiki/GLUT4

41. 고지방식이 백서에서 운동훈련이 인슐린 감수성 및 골격근 세포내 포도당대사에 미치는 영향 - Diabetes & Metabolism Journalhttps://www.e-dmj.org/upload/pdf/dmj-22-2-231.pdf

42. 당뇨병 : 제17권 제2호 1993 - NIDDM의 인슐린 저항증과 제4형 당이동체 (GLUT 4)https://www.e-dmj.org/upload/pdf/dmj-17-2-157.pdf

43. 인슐린 신호 및 RTK: 개요https://www.assaygenie.kr/blog/insulin-signalling-and-rtks-kr

44. 인슐린 저항성과 발기부전 - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/1020kju/kju-47-917.pdf

45. 인슐린과 심혈관질환 - 성균관의대 강북삼성병원 내분비내과https://e-enm.org/upload/pdf/44502805.pdf

46. 대사증후군과 심혈관 위험인자의 관련성https://kjfm.or.kr/upload/pdf/Jkafm026-10-04.pdf

47. 제2형 당뇨병환자에서 대사증후군과 만성 합병증과의 관계https://www.e-dmj.org/upload/pdf/kdj-33-392.pdf

48. 대사증후군의 현황https://www.ekjm.org/upload/42837295.pdf

49. 비알코올성 지방간 환자에서 대사증후군의 유병률https://www.e-cmh.org/upload/pdf/27401604.pdf

50. 우리나라 성인의 인슐린 저항성과 관련된 영양소 및 식품군 섭취: 제 4기 국민건강영양조사 자료를 활용하여 - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/0124kjn/kjn-46-61.pdf

51. 대사증후군과 인슐린저항성 평가를 위한 시상복부 직경의 유용성https://www.kjfm.or.kr/upload/pdf/Jkafm032-01-07.pdf

52. 정상 성인 남성에서의 대사증후군과 인슐린 저항성과의 관련성: IDF 새로운 진단기준과 NCEP-ATP IIIhttps://www.kjfm.or.kr/upload/pdf/Jkafm027-10-05.pdf

53. 한국인의 인슐린저항성증후군https://e-enm.org/upload/pdf/44500201.pdf

54. 인슐린저항성의 정의https://www.koreascience.kr/article/JAKO200372324257202.pdf

55. 비알코올성 지방간질환과 아디포넥틴https://www.e-dmj.org/upload/pdf/kdj-32-98.pdf

56. 당뇨병이 없는 정상체중의 성인에서 비알콜성 지방간과 인슐린 저항성과의 연관성https://www.ekjm.org/upload/42833022.pdf

57. '다낭성난소증후군' 불임부터 당뇨, 지방간, 탈모까지 - 의학신문http://www.bosa.co.kr/news/articleView.html?idxno=2155410

58. 다낭난소증후군과 인슐린저항성https://www.e-dmj.org/upload/pdf/kdj-32-1.pdf

59. 진료질환정보( 다낭성 난소 증후군 [polycystic ovary syndrome, PCOS] ) | 서울대학교어린이병원http://child.snuh.org/health/nMedInfo/nView.do?category=DIS&medid=AA000273

60. 다낭성 난소 증후군(Polycystic ovary syndrome) | 질환백과 | 의료정보 - 서울아산병원https://www.amc.seoul.kr/asan/healthinfo/disease/diseaseDetail.do?contentId=31833

61. 다낭성 난소증후군 [Polycystic ovarian syndrome] | 건강정보 - 세브란스병원https://sev.severance.healthcare/health/encyclopedia/disease/body_board.do?mode=view&articleNo=66607&title=%EB%8B%A4%EB%82%AD%EC%84%B1+%EB%82%9C%EC%86%8C%EC%A6%9D%ED%9B%84%EA%B5%B0+%5BPolycystic+ovarian+syndrome%5D

62. KoreaMed Synapsehttps://synapse.koreamed.org/articles/1516079614

63. 당뇨병·비만 원인 '인슐린 저항성', 우울증 위험까지 끌어올려 [건강한겨레]https://www.hani.co.kr/arti/hanihealth/medical/1221720.html

64. 문제는 '인슐린저항성', 개선 어떻게? - 헬스조선https://m.health.chosun.com/svc/news_view.html?contid=2021111101839

65. '이것' 높을수록 당뇨 발병 위험↑…당뇨 있다면 피해야 하는 음식 5 > 건강정보 | 성가롤로병원https://www.stcarollo.or.kr/0401/2126

66. 식단관리가 중요한 당뇨, 좋은음식과 나쁜음식은? > 건강정보 | 수원 더웰병원https://www.thewellhospital.com/bbs/board.php?bo_table=health_info&wr_id=42&page=12

67. 인슐린 저항성을 낮추는 최고의 방법 1가지 - 웰빙썸https://wellbeingthumb.co.kr/article/%EA%B1%B4%EA%B0%95-%EB%A7%A4%EA%B1%B0%EC%A7%84/8/711/

68. 당뇨병 막기...인슐린 저항성 개선 식사 팁 - 코메디닷컴https://kormedi.com/1576060/

69. 당뇨에 좋은 음식 5가지 vs 안 좋은 음식 - 닥터나우https://doctornow.co.kr/content/magazine/97cdc9c0a5754a39a3c1f0edadda44db

70. 식단으로 혈당 수치를 개선하는 방법https://www.mskcc.org/ko/pdf/cancer-care/patient-education/how-to-improve-your-blood-sugar-with-your-diet

71. 혈당 관리에 좋은 음식 Best 5 - 브로리코몰https://www.igcmall.com/health-7/

72. 인슐린 저항성을 낮추는 5가지 필수 식품, 당신의 식단에 추가해야 할 이유는? - Daumhttps://v.daum.net/v/KRGS8p8tNl

73. 당뇨 있을 때...좋은 식품 vs 나쁜 식품 - 코메디닷컴https://kormedi.com/1561611/

74. 식단으로 혈당 수치를 개선하는 방법https://www.mskcc.org/ko/cancer-care/patient-education/how-to-improve-your-blood-sugar-with-your-diet

75. 인슐린저항성 개선에 도움되는 5가지 음식https://hyperthermia.tistory.com/1276

76. 췌장 인슐린 분비를 촉진하는 한국 전통 발효음식 '이것'! | 당뇨문의 : 1644-5178https://www.youtube.com/watch?v=lTEf-6VBKnw

77. 테마칼럼 - 대사증후군이란 만성적인 대사 장애로 인해 비만(복부비만), 이상지질혈증, 혈당 증가, 혈압 증가 중 한 사람에게 3가지 이상의 증상이 나타나는 경우를 말합니다. 서구식 생활습관으로 인해 체지방은 늘고 근육이 감소하는 비만 체형의 증가와 대사증후군의 발생은 연관성이 높은 것으로 알려져 있습니다. 따라서 대사증후군과 인슐린 저항성을 개선하기 위해서는 운동과 식이조절로 비만에서 벗어나는 것은 물론, 근육이 줄어들지 않도록 노력하는 것 또한 중요합니다. - 테마칼럼 - 국민건강보험공단https://www.nhis.or.kr/magazin/mobile/201501/sub04.html

78. 집에서 꾸준히 하면 '혈당' 내려가는 운동법 2가지 - 의학정보 > 강좌http://www.gysarang.com/Module/News/Lecture.asp?MODE=V&SRNO=27181

79. 운동이 당대사에 미치는 영향 - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/0178jkd/jkd-12-21.pdf

80. 운동이 당뇨병환자의 심혈관질환에 미치는 영향 (유산소 vs. 저항성) - KoreaMed Synapsehttps://synapse.koreamed.org/upload/synapsedata/pdfdata/0178jkd/jkd-12-25.pdf

81. 밥 먹고 10분만 제자리서 '이 운동'… 혈당 조절 효과 커 - 헬스조선https://m.health.chosun.com/svc/news_view.html?contid=2024043001866

82. 잠들기 어려울 때 3대 호르몬 관리법 > 칼럼 - 닥터박민수닷컴https://www.drparkminsu.com/column/108?sfl=wr_tag&stx=%EB%A9%B4%EC%97%AD&sop=and

83. 인슐린 저항성은 무엇?...당뇨병 피하기 위해 알아야 할 것들 - 코메디닷컴https://kormedi.com/2732792/

84. 당뇨교육실 - 삼성서울병원http://www.samsunghospital.com/dept/main/bbsView.do?CID=21678&cPage=1&MENU_ID=005045&DP_CODE=DM

85. 인슐린 저항성을 극복하는 확실한 8가지 해결방법(비만, 당뇨, 만성피로, 만성질환의 근본해결은 이것부터) - YouTubehttps://www.youtube.com/watch?v=9ayEDY-5S6M

86. 인슐린 저항성 개선 보충제 7가지 | 웰니스 허브 - iHerbhttps://kr.iherb.com/blog/insulin-resistance-causes-signs-supplements/1297