Hyperinsulinemia Explained: The Earliest Stage of Metabolic Dysfunction

Most people have never heard of hyperinsulinemia. Yet it is almost certainly the most common metabolic abnormality in Western populations — and the one that is least routinely tested for.

It does not cause symptoms. It does not appear on a standard blood panel unless you specifically request a fasting insulin test. And by the time it progresses to prediabetes, type 2 diabetes, or cardiovascular disease, it has typically been silently driving dysfunction for a decade or more.

Hyperinsulinemia means chronically elevated insulin in the blood. It is not a diagnosis most clinicians will give you. It is not a disease with a clear ICD code. But it is, in the words of Gerald Reaven — the Stanford endocrinologist who spent decades mapping insulin resistance — the earliest detectable metabolic abnormality in the long trajectory from metabolic health to type 2 diabetes and cardiovascular disease.

This article explains what hyperinsulinemia is, why it develops, what it does to your body across multiple organ systems, and — critically — how to detect it before it silently causes damage.

Clinical Perspective: What I See in Practice

I first encountered hyperinsulinemia not in a patient’s chart but in my own lab results.

In 2016 I was experiencing what I would later recognize as a textbook compensatory hyperinsulinemia picture — fatigue, metabolic symptoms, a metabolism working harder than it should. At the time I did not yet have the framework to name it correctly. That framework came through the work of researchers like Benjamin Bikman, Joseph Kraft, and Gerald Reaven, and through a realization that slowly became impossible to ignore in my own clinical practice: the patients in front of me were not primarily suffering from high blood sugar. They were suffering from high insulin. The glucose was a downstream consequence. The insulin was the upstream driver. And nobody — not their GPs, not the specialists, not the nutrition science curriculum I trained in at a German university — was talking about it in those terms.

At university, the focus was almost entirely on sugar. The mechanistic pathway from hyperinsulinemia to insulin resistance to metabolic syndrome was touched on briefly if at all. The clinical training was oriented around glucose thresholds, HbA1c targets, and medication titration. Hyperinsulinemia as a distinct, measurable, actionable clinical entity was essentially absent from the conversation. I have never — in years of clinical practice in Germany — had a GP refer a patient to me with hyperinsulinemia listed as a concern. Not once. The word does not appear in referral letters. It does not appear in discharge summaries. In most cases it does not appear in the patient’s awareness at all.

I remember a moment several years ago in a Facebook group for people with type 2 diabetes. I wrote that every time you eat, your pancreas releases insulin. The response was not curiosity. It was hostility. People who were managing type 2 diabetes with oral medication — some for years — did not know what insulin was or what it did in their bodies. That is not a failure of individual patients. It is a systemic failure of how metabolic disease is communicated and treated.

What I see in practice is the consequence of that failure arriving, typically, in a person’s late 40s or 50s. The downstream effects — fat storage dysfunction, dyslipidemia, fatty liver, hypertension, hormonal disruption, cognitive decline — have been developing for a decade or more. Every one of them is connected to the same upstream signal. When I explain that connection to patients, the reaction is not just surprise. It is a specific kind of frustration — the frustration of someone who was never told that the system they trusted to monitor their health was not looking at the right thing.

The outcomes data from my practice tells the clearest version of this story. One patient arrived with an HbA1c of 9.2%, fasting glucose of 215 mg/dL, triglycerides of 240 mg/dL, and three medications. Within the program, HbA1c came down to 6.5%, fasting glucose to 112 mg/dL, triglycerides to 120 mg/dL — halved — and medications reduced from three to one. Another patient presented with fasting insulin of 18 µIU/mL and HbA1c of 6.1%. After the protocol — low-carbohydrate animal-based nutrition, structured intermittent fasting, resistance training, sleep optimization, and elimination of ultra-processed foods — fasting insulin dropped to 7 µIU/mL and HbA1c to 5.2%. Eight kilograms of body weight lost. GLP-1 discontinued. The patient’s own words: “I stopped fighting my body and started understanding it.”

These are not exceptional cases. They are what consistently happens when the root cause is identified and addressed rather than managed downstream.

If I could communicate one thing to every GP in Germany it would be this: stop being obsessed with blood glucose alone and start ordering fasting insulin. Take elevated triglycerides seriously as a metabolic signal — not a footnote. Take NAFLD seriously as an early marker of insulin resistance, not a late complication of obesity. The information needed to identify hyperinsulinemia early is available, inexpensive, and actionable. The decision not to order it is costing patients the one thing that cannot be recovered once it is gone — time.

What Is Hyperinsulinemia?

Hyperinsulinemia literally means ‘too much insulin in the blood.’ In clinical terms, it refers to a state in which fasting insulin levels are chronically elevated above what is required for normal metabolic function — typically defined as fasting insulin above 10–15 µIU/mL, though the physiologically optimal range is considerably lower.

To understand why this matters, it helps to understand what insulin is supposed to do — and what happens when it is chronically overproduced.

Normal Insulin Physiology

Insulin is secreted by the beta cells of the pancreas in response to rising blood glucose — primarily after eating carbohydrates. Its job is to signal cells in the liver, skeletal muscle, and fat tissue to take up glucose from the bloodstream, either for immediate energy use or for storage as glycogen or fat.

In a metabolically healthy individual, this process is highly efficient. A small insulin signal is sufficient to keep blood glucose within a tight range. Between meals and during fasting, insulin levels drop to a low baseline — typically below 5 µIU/mL. This low fasting state is what allows the body to access stored fat for energy.

Hyperinsulinemia occurs when this system is no longer efficient. When cells become less responsive to insulin — a state called insulin resistance — the pancreas compensates by secreting more insulin to achieve the same glucose-lowering effect. Blood glucose may remain normal for years, but insulin quietly climbs. This is the defining pattern of early metabolic dysfunction.

The Relationship Between Hyperinsulinemia and Insulin Resistance

Hyperinsulinemia and insulin resistance are tightly linked — but they are not the same thing. Insulin resistance is a cellular state: the reduced ability of cells to respond appropriately to insulin’s signal. Hyperinsulinemia is the hormonal consequence: the pancreas secreting excess insulin to override that resistance.

They also exist in a bidirectional relationship. Insulin resistance drives hyperinsulinemia — but hyperinsulinemia also drives further insulin resistance. Chronic overexposure to insulin causes cells to downregulate their insulin receptors, deepening resistance and requiring even higher insulin output to maintain glucose control. This self-reinforcing cycle is one of the central mechanisms driving progressive metabolic dysfunction.

A Brief Recap: Why Fasting Insulin Is the Key Marker

If you have read our previous article on fasting insulin optimal ranges, you will recognise this framework. If not, here is the essential context.

Most laboratory reference ranges flag fasting insulin as ‘normal’ anywhere below 17–25 µIU/mL, depending on the assay. These ranges are derived from population averages — not from research on optimal metabolic health. In populations where insulin resistance is common, using the average to define ‘normal’ sets the bar far too low.

Research — including seminal work by Joseph Kraft in the 1970s and subsequent large epidemiological studies — consistently demonstrates that insulin resistance, and with it compensatory hyperinsulinemia, frequently exists in individuals with fasting insulin values between 8 and 12 µIU/mL. Values that will pass unremarked on any standard blood panel.

The following thresholds reflect the clinically actionable framework used in this practice, based on current evidence:

How Hyperinsulinemia Develops: The Compensatory Spiral

Hyperinsulinemia does not emerge overnight. It develops gradually, over years or decades, driven by a combination of lifestyle factors that progressively impair cellular insulin sensitivity.

Stage 1: Reduced Cellular Insulin Sensitivity

The process typically begins in skeletal muscle — the body’s primary site of insulin-mediated glucose disposal. Chronic dietary carbohydrate excess, physical inactivity, accumulation of intramyocellular fat, and low-grade systemic inflammation all impair insulin receptor signalling in muscle tissue.

As muscle cells become less responsive, more insulin is required to clear the same amount of glucose from the bloodstream after a meal. The pancreas obliges, secreting higher amounts of insulin post-meal — a state called postprandial hyperinsulinemia, which precedes the more clinically apparent elevation of fasting insulin.

Stage 2: Compensatory Fasting Hyperinsulinemia

Over time, as liver insulin resistance develops alongside muscle resistance, the pancreas begins secreting elevated insulin even in the fasted state. This is because the liver — which is normally suppressed from producing glucose by insulin signalling — becomes resistant to insulin’s inhibitory effect and continues releasing glucose into the bloodstream. The pancreas responds by maintaining higher baseline insulin output.

This is the stage at which fasting insulin becomes elevated. It is also the stage at which the self-reinforcing cycle becomes established: chronic hyperinsulinemia further downregulates insulin receptors across tissues, deepening resistance and pushing insulin output even higher.

Stage 3: Beta Cell Strain and Eventual Failure

In most people, the pancreas can sustain compensatory hyperinsulinemia for many years or decades before beta cell function begins to decline. Glucose remains normal throughout this window — which is precisely why standard glucose-based screening fails to detect it.

Eventually, if the underlying drivers are not addressed, beta cell capacity begins to fail. Insulin output can no longer keep pace with the degree of resistance. Fasting glucose begins to rise, postprandial glucose spikes become prolonged, and the clinical picture of prediabetes — then type 2 diabetes — emerges. By this point, beta cell function is already significantly compromised, sometimes by 50% or more.

This is why early detection through fasting insulin is so clinically meaningful. Identifying hyperinsulinemia at Stage 2 — before glucose becomes abnormal — represents a window of intervention that standard screening misses almost completely.

What Drives Hyperinsulinemia: Root Causes

Hyperinsulinemia is a downstream signal. Understanding its upstream drivers is what makes targeted intervention possible.

• Chronic dietary carbohydrate excess: Particularly refined carbohydrates and sugar. High-frequency insulin secretion from a high-glycemic diet reduces cellular insulin sensitivity over time — the most direct and well-established driver.
• Physical inactivity and low muscle mass: Skeletal muscle accounts for approximately 80% of insulin-mediated glucose disposal. Low muscle mass and sedentary behaviour substantially increase the insulin load required to manage blood glucose.
• Visceral adiposity: Excess intra-abdominal fat releases free fatty acids and pro-inflammatory cytokines — including TNF-alpha and IL-6 — that directly impair insulin receptor signalling in liver and muscle.
• Sleep disruption: Even one night of poor sleep measurably increases insulin resistance. Chronic sleep deprivation elevates cortisol, disrupts glucose regulation, and is an underrecognised driver of fasting hyperinsulinemia.
• Chronic psychological stress: Cortisol is counter-regulatory to insulin. Sustained cortisol elevation drives hepatic gluconeogenesis and reduces peripheral insulin sensitivity — a mechanism that helps explain the metabolic consequences of long-term stress.
• Ultra-processed food exposure: Independent of macronutrient content, ultra-processed foods promote systemic inflammation and gut dysbiosis, both of which impair insulin signalling pathways.

What Chronically Elevated Insulin Does to the Body

Insulin is not merely a glucose-regulating hormone. It is one of the most pleiotropic — wide-acting — hormones in the human body. When it is chronically elevated, its effects extend far beyond blood sugar control. This is why hyperinsulinemia is implicated in a range of conditions that, superficially, may appear unrelated.

Fat Storage and Body Composition

Insulin is profoundly anti-lipolytic — it directly inhibits the breakdown and mobilisation of stored fat (a process called lipolysis). When insulin is chronically elevated, even in a caloric deficit, fat mobilisation is significantly impaired. This is one of the most clinically relevant and underappreciated consequences of hyperinsulinemia.

It explains why some individuals struggle disproportionately with fat loss despite controlling caloric intake, exercising regularly, and ‘doing everything right.’ If fasting insulin remains elevated, the hormonal environment is chronically tilted away from fat oxidation and toward fat storage.

Beyond this, chronic hyperinsulinemia preferentially promotes visceral fat accumulation — the metabolically active intra-abdominal fat that itself drives further insulin resistance. This creates a second self-reinforcing cycle: hyperinsulinemia promotes visceral fat deposition, and visceral fat deepens hyperinsulinemia.

Cardiovascular Risk

The relationship between hyperinsulinemia and cardiovascular disease is both independent and mechanistically well-characterised. Elevated insulin exerts direct atherogenic effects beyond its role in glucose metabolism.

Key mechanisms include:

• Dyslipidemia: Chronic hyperinsulinemia promotes hepatic VLDL triglyceride synthesis and suppresses HDL cholesterol — producing the classic dyslipidemic pattern (elevated triglycerides, low HDL) that is strongly associated with cardiovascular risk. This is why the triglyceride-to-HDL ratio is a robust clinical proxy for insulin resistance.
• Endothelial dysfunction: Insulin normally has vasodilatory effects mediated through nitric oxide. In the context of insulin resistance, this pathway is selectively impaired while the pro-proliferative effects of insulin on vascular smooth muscle remain intact — promoting arterial stiffness and atherosclerosis.
• Sympathetic nervous system activation: Hyperinsulinemia directly activates the sympathetic nervous system, contributing to elevated blood pressure — an effect that is clinically well-documented in populations with insulin resistance.

Large longitudinal studies, including data from the Quebec Cardiovascular Study, have demonstrated that fasting hyperinsulinemia independently predicts incident coronary artery disease — even after adjusting for glucose, lipids, and blood pressure. Insulin itself, not just the downstream consequences of glucose dysregulation, appears to be directly atherogenic.

Progression to Type 2 Diabetes

The trajectory from hyperinsulinemia to type 2 diabetes is not inevitable — but it is well-defined and well-evidenced. Hyperinsulinemia is Stage 1 of that trajectory. Understanding this sequence is clinically important because every stage except the final one is reversible with appropriate intervention.

The sequence runs approximately as follows:

• Cellular insulin resistance develops (muscle, then liver)
• Compensatory hyperinsulinemia maintains normal glucose — sometimes for decades
• Progressive beta cell stress and gradual loss of function
• Fasting glucose begins to rise (impaired fasting glucose)
• Postprandial glucose dysregulation becomes apparent (impaired glucose tolerance)
• Type 2 diabetes: sustained hyperglycaemia with overtly inadequate insulin response

The data from the Whitehall II study and similar long-term cohorts confirm that individuals in the top quartile of fasting insulin have substantially elevated risk of developing type 2 diabetes over 10-year follow-up — even within the ‘normal’ glucose range.

The clinical implication is direct: addressing hyperinsulinemia at Stage 2 — before glucose becomes abnormal — is incomparably more effective than treating type 2 diabetes once established.

Cognitive Decline and Brain Insulin Resistance

Perhaps the most significant — and least widely appreciated — consequence of chronic hyperinsulinemia is its effect on the brain.

The brain is an insulin-sensitive organ. Insulin receptors are densely expressed in the hippocampus and frontal cortex — regions critical for memory consolidation, executive function, and learning. Insulin signaling in the brain modulates synaptic plasticity, neuronal glucose uptake, and the clearance of amyloid-beta peptides, the proteins whose accumulation is a hallmark of Alzheimer’s disease pathology.

Chronic systemic hyperinsulinemia, followed by progressive cerebral insulin resistance, impairs all of these functions. The brain’s ability to clear amyloid-beta is particularly relevant: insulin and amyloid-beta compete for the same degrading enzyme (insulin-degrading enzyme, IDE). Chronically elevated insulin effectively outcompetes amyloid-beta for clearance, allowing it to accumulate.

This mechanism is one of the reasons some researchers now refer to Alzheimer’s disease as “Type 3 Diabetes” — a term coined by Suzanne de la Monte at Brown University to reflect the centrality of impaired cerebral insulin signalling in Alzheimer’s pathogenesis. While this framing remains a subject of active research debate, the association between insulin resistance and cognitive decline is now well-established across multiple large epidemiological studies.

A 2017 study published in JAMA Neurology found that insulin resistance in midlife was associated with significantly greater amyloid deposition and cognitive decline decades later — independent of traditional cardiovascular risk factors. The implication is that metabolic health in middle age directly shapes cognitive reserve in older age.

How to Detect Hyperinsulinemia: Testing and Interpretation

Fasting Insulin: The Primary Marker

Fasting insulin measured after a 10–12 hour fast is the most accessible and clinically informative single test for identifying hyperinsulinemia. It directly quantifies the pancreatic output required to maintain baseline glucose — and is therefore a direct proxy for the degree of systemic insulin resistance.

Testing conditions matter: any caloric intake — including milk in coffee — will stimulate insulin secretion and invalidate the result. Water is fine. The test should be conducted before significant physical exertion.

As noted above, a fasting insulin below 5 µIU/mL is optimal. Values above 10 µIU/mL in a non-fasted-for-longer-than-normal individual represent early hyperinsulinemia that warrants clinical attention.

HOMA-IR: Adding Glucose to the Picture

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) combines fasting insulin and fasting glucose: HOMA-IR = (Fasting Insulin [µIU/mL] × Fasting Glucose [mmol/L]) ÷ 22.5. A value below 1.0 is optimal; above 2.0 indicates significant insulin resistance; above 2.9 is associated with substantially elevated cardiovascular and metabolic risk.

HOMA-IR is useful because it accounts for both components of the compensation mechanism. However, in early hyperinsulinemia where fasting glucose is still normal, fasting insulin alone may be the more sensitive indicator.

Supporting Markers

Fasting insulin should not be interpreted in isolation. The full metabolic picture includes:

• Fasting glucose and HbA1c: to identify whether glucose dysregulation has already begun
• Triglycerides and HDL (triglyceride-to-HDL ratio): a strong clinical proxy for insulin resistance — a ratio above 2.0 (using mg/dL) or above 0.9 (mmol/L) is clinically significant
• Waist circumference and body composition: visceral fat is both a cause and a consequence
• Blood pressure: elevated insulin activates the sympathetic nervous system and promotes sodium retention — hypertension is frequently a downstream marker of insulin resistance

What to Do About Hyperinsulinemia: Evidence-Based Interventions

Hyperinsulinemia is not a fixed state. It is a reversible signal. The evidence for lifestyle intervention in reducing fasting insulin is robust — and the mechanisms are well understood.

Dietary Approach

Reducing dietary carbohydrate load — particularly refined carbohydrates, sugar, and high-glycemic foods — is the most direct lever for lowering fasting insulin. Every carbohydrate-containing meal stimulates insulin secretion. Reducing carbohydrate frequency and glycemic load reduces the insulin burden directly.

Low-carbohydrate and ketogenic dietary patterns demonstrate the strongest and most rapid reductions in fasting insulin of any dietary intervention studied. Time-restricted eating and intermittent fasting lower fasting insulin by extending the overnight fasting window — allowing insulin to remain suppressed for longer periods and improving receptor sensitivity through periodic insulin withdrawal.

Exercise: Quality and Type Matter

Resistance training is the most mechanistically targeted exercise intervention for insulin resistance. Building skeletal muscle mass directly increases the body’s capacity to dispose of glucose without insulin involvement, through GLUT4 translocation — a non-insulin-mediated pathway that remains functional even in resistant muscle.

High-intensity interval training (HIIT) also demonstrates significant reductions in fasting insulin across multiple randomised controlled trials, likely through a combination of GLUT4 upregulation, improved mitochondrial density, and reduced visceral fat.

Even a single session of moderate aerobic exercise transiently improves insulin sensitivity for 24–48 hours — an effect that accumulates with consistent training frequency.

Sleep and Stress: The Underrecognised Levers

Optimising sleep quality and duration to 7–9 hours is a non-negotiable component of any serious intervention on hyperinsulinemia. The effect of sleep deprivation on insulin resistance is rapid and measurable — and no dietary or exercise intervention can fully compensate for chronically poor sleep.

Chronic psychological stress maintains elevated cortisol, which directly drives hepatic glucose output and peripheral insulin resistance. Evidence-based stress reduction approaches — whether structured cognitive-behavioural techniques, consistent parasympathetic activation through breath or movement, or simply reducing chronic stressors — have a meaningful and underutilised place in metabolic management.

Eliminate Industrial Seed Oils, HFCS, and Ultra-Processed Foods

The modern food supply contains several compounds that drive insulin resistance through a distinct and underappreciated pathway: gut-mediated systemic inflammation. Industrial seed oils (high in omega-6 linoleic acid), high-fructose corn syrup, and ultra-processed foods disrupt the intestinal barrier, increasing its permeability to lipopolysaccharide (LPS) — an endotoxin derived from gram-negative gut bacteria.

Elevated circulating LPS triggers a chronic low-grade inflammatory response via toll-like receptor 4 (TLR4) activation, which directly impairs insulin signalling in the liver. This hepatic insulin resistance forces compensatory hyperinsulinemia — raising fasting insulin even in individuals who otherwise eat moderate carbohydrate loads. Eliminating these compounds reduces endotoxin translocation, lowers inflammatory tone, and restores hepatic insulin sensitivity through a pathway entirely separate from carbohydrate restriction alone.

Prioritize Protein to Counter Metabolic Slowing With Age

Ageing is accompanied by a progressive decline in metabolic rate, driven largely by the loss of skeletal muscle mass — sarcopenia. As muscle is the primary site of insulin-stimulated glucose disposal, this loss directly worsens insulin sensitivity and contributes to rising fasting insulin in older adults, independent of changes in diet or activity.

Prioritising dietary protein — particularly leucine-rich sources such as meat, eggs, and dairy — stimulates muscle protein synthesis and attenuates age-related muscle loss. Maintaining or rebuilding muscle mass preserves metabolic rate, restores glucose disposal capacity, and reduces the insulin demand placed on the pancreas. Protein also has a minimal direct effect on insulin secretion compared to carbohydrate, making a high-protein dietary pattern doubly advantageous in the context of hyperinsulinemia. For older adults especially, protein intake is not a secondary consideration — it is a primary metabolic intervention.

A Note on Uncertainty

The clinical thresholds cited in this article are derived from epidemiological evidence, mechanistic research, and clinical observation — not from a single definitive randomised controlled trial. Different clinicians and researchers draw slightly different lines, and individual variability is real.

What the evidence consistently shows is that lower fasting insulin — within a physiological range — is associated with better long-term metabolic, cardiovascular, and cognitive outcomes. The direction of the evidence is clear even where precise thresholds remain debated.

Fasting insulin is also only one input into a broader clinical picture. A value of 6 µIU/mL in an individual with visceral adiposity, poor dietary patterns, and a sedentary lifestyle tells a different story than the same number in a lean, active person. Context and trajectory always matter more than a single data point.

Next Steps

If you have not yet measured your fasting insulin, request it at your next blood draw alongside fasting glucose. It is inexpensive, widely available, and provides information that standard metabolic screening systematically misses.

If you already have a result and want to understand what it means in the context of your full metabolic picture — including glucose, lipids, body composition, and clinical history — the next step is a structured metabolic assessment.

The question is not whether you have ‘normal’ insulin. The question is whether your metabolic system is functioning optimally — and what needs to change to protect it over the long term.

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About the Author

Morteza Ariana is a State-Certified Functional Nutritionist based in Germany, specializing in insulin resistance, type 2 diabetes, and root-cause metabolic restoration. He holds advanced training in systems-based physiology and has worked with patients across the U.S. and Europe for over 10 years.

His clinical framework is built around a core principle that mainstream medicine consistently overlooks: chronically elevated insulin — not blood glucose — is the earliest and most actionable driver of metabolic disease. That conviction was shaped in part by his own experience with hyperinsulinemia in 2016, and deepened through a decade of clinical practice and the study of leading researchers in metabolic medicine including Benjamin Bikman, Joseph Kraft, Gerald Reaven, Jason Fung, and Stephen Phinney.

His work focuses on identifying and correcting the upstream metabolic signals — insulin load, liver-gut axis dysfunction, circadian misalignment, and micronutrient gaps — that standard screening misses entirely. Patient outcomes are documented, anonymized, and published on this site.

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Key References

1. Reaven GM. Role of insulin resistance in human disease. Diabetes. 1988;37(12):1595–1607.

2. Kraft JR. Detection of diabetes mellitus in situ (occult diabetes). Laboratory Medicine. 1975;6(2):10–22.

3. Despres JP, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. New England Journal of Medicine. 1996;334(15):952–957.

4. Whitehall II Study investigators. Fasting insulin and risk of type 2 diabetes. Diabetologia. 2007;50(12):2481–2488.

5. de la Monte SM, Wands JR. Alzheimer’s disease is type 3 diabetes — evidence reviewed. Journal of Diabetes Science and Technology. 2008;2(6):1101–1113.

6. Willette AA, et al. Insulin resistance predicts brain amyloid deposition in late middle-aged adults. JAMA Neurology. 2015;72(6):657–665.

7. Abdul-Ghani MA, DeFronzo RA. Pathogenesis of insulin resistance in skeletal muscle. Journal of Biomedicine and Biotechnology. 2010;2010:476279.

8. Facchini FS, et al. Insulin resistance as a predictor of age-related diseases. Journal of Clinical Endocrinology & Metabolism. 2001;86(8):3574–3578.