REVIEW ARTICLE Year : 2023  |  Volume : 50  |  Issue : 1  |  Page : 19-22

Insulin resistance and its detection tools: A narrative review

Janhavi Mahajan, Sourya Acharya, Sunil Kumar
Department of Medicine, Datta Meghe Institute of Medical Sciences (Deemed to be University), Sawangi (Meghe), Wardha, Maharashtra, India

Date of Submission15-Jun-2022Date of Decision25-Aug-2022Date of Acceptance11-Sep-2022Date of Web Publication24-Mar-2023

Correspondence Address:
Janhavi Mahajan
Department of Medicine, Datta Meghe Institute of Medical Sciences (Deemed to be University), Sawangi (Meghe), Wardha, Maharashtra
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/jss.jss_122_22

Insulin resistance (IR) is a defining feature of obesity, diabetes, and cardiovascular disease, and it contributes to many of the metabolic syndrome's abnormalities. Although our understanding of IR has vastly increased over time, several parts of its assessment continue to elude researchers and doctors. Although the quantitative assessment of insulin sensitivity is not regularly utilized in biochemical investigations for diagnostic purposes, the growing importance of IR has led to further research into its application. IR must be assessed in a number of clinical situations when insulin sensitivity is reduced. IR is being studied more and more in numerous disease states to help researchers better understand its pathophysiology, etiology, and implications. The gold standard approach for determining insulin sensitivity is the hyperinsulinemic euglycemic glucose clamp, although it is impractical due to its labor- and time-intensive nature. As a result, a variety of surrogate indices have been used to make determining IR easier and more accurate. The goal of this study is to highlight different elements and approaches for present and future insulin sensitivity/resistance measurements. Understanding and exploiting the condition will be aided by a thorough understanding of these signs.

Keywords: Diabetes, diagnostic tools, insulin resistance

How to cite this article:
Mahajan J, Acharya S, Kumar S. Insulin resistance and its detection tools: A narrative review. J Sci Soc 2023;50:19-22
  Introduction 

Insulin is a crucial factor in maintaining glucose homeostasis. Insulin resistance (IR) develops as a result of a combination of genetic and environmental factors. IR causes reduced glucose tolerance and is a key pathophysiological factor in diabetes development.[1] Furthermore, many of the metabolic problems linked with metabolic syndrome/syndrome X are caused by IR. IR increases the prevalence of atherogenic small dense low-density lipoprotein (LDL) particles, which increases the prevalence of atherogenic small dense LDL particles. The pathogenesis of dyslipidemia, glucose intolerance, persistent subclinical inflammation, and hypertension in metabolic syndrome is based on central obesity and IR. IR is defined as a state in which more insulin is required than normal to get a quantitatively normal response.[2] IR measurement has moved from its position in diabetes pathogenesis to an even more essential role.

The inflammatory cascade plays a significant part in the mechanism behind IR, which involves a complicated network of glucose and lipid metabolism. Insulin's main activities are anti-lipolysis in adipose tissue and lipoprotein lipase stimulation.[3] Through the action of the cyclic AMP-dependent enzyme hormone sensitive lipase, obesity-related increased adipose tissue mass mobilizes free fatty acids (FFAs) in circulation. FFAs are also released in tissues as a result of lipoprotein lipase's lipolysis of TG-rich lipoproteins.[4] Excess fatty acids cause IR in insulin-sensitive tissue by increasing substrate availability and altering downstream signaling.[5] Increased lipolysis of accumulated TG in adipose tissue creates more fatty acids when IR develops. Insulin's anti-lipolytic activity is inhibited by increasing FFA levels. The significance of innate immunity and infection in the development of IR has also been proposed, and it has been shown to predict the development of diabetes mellitus type II.[6],[7] IR, metabolic syndrome, and atherosclerosis events all have an inflammatory component in common. The major factor that leads to decreased insulin action is the presence of low-grade systemic inflammation.[8] This narrative review discussed the various diagnostic tools for IR.

  Methods 

The following goals are being pursued with this review: To assess the diagnostic tools for IR [Figure 1].

The electronic databases PubMed, Medline, Embase, and Google were used to conduct a literature search in English. The terms Diagnostic Tools OR IR were used in the search. The writers' personal knowledge and experience in the topic aided in the archiving of pertinent publications. The present review includes articles that meet the following criteria: (1) English-language studies are included; (2) Studies published in the last 10 years are also included; and (3) Studies that are solely focused on IR are included.

  Discussion 

A marker is a measurable variable that can represent the underlying illness pathophysiology, forecast future occurrences, and signal therapy response. It can be identified in a biological sample or detected by tissue imaging. Early target organ damage can be detected using markers.[9] Validated risk-assessment techniques currently do not account adequately for the elevated risk variables associated with metabolic syndrome.[10] As a result, identifying indicators for this disease is critical.

The estimation of IR in humans is a hot topic of research. It is critical to create animal models that are suitable for studying the epidemiology, pathophysiological causes, therapeutic intervention outcomes, and clinical outcomes of individuals with IR. IR is a well-known independent predictor of a variety of illnesses. IR develops long before any illness symptoms arise. Because hyperinsulinemia can lie untreated for a long time, the chance of developing other syndrome components and disorders increases. Early detection and therapy of this metabolic syndrome can help prevent serious health problems.[11]

There are many other important physiological targets of insulin, such as the brain, pancreatic-cells, heart, and vascular endothelium, that help to coordinate and couple metabolic and cardiovascular homeostasis under healthy conditions,[12],[13],[14],[15] in addition to maintaining whole body glucose homeostasis and promoting efficient glucose utilization.[12] As a result, an accurate approach for quickly assessing insulin sensitivity and tracking changes after therapeutic intervention is needed.

The euglycemic hyperinsulinemic clamp technique is a direct method of estimating IR among the instruments used to describe IR and quantify whole body insulin action. Because this necessitates insulin infusion and periodic blood samples, simple, accessible measures for assessing insulin sensitivity are required. The majority of large-scale epidemiological studies simply link fasting insulin levels to the desired outcome. Here are a few diagnostic tools listed that are used to assess the IR.

Oral glucose tolerance test

The oral glucose tolerance test (OGTT) is a simple test that is frequently used in medical practise to diagnose glucose intolerance and type 2 diabetes.[16] It entails the delivery of glucose to determine how quickly it is eliminated from the bloodstream. It refers to the body's ability to use glucose after a glucose load. Blood glucose levels are measured at 0, 30, 60, and 120 min after a standard oral glucose load (75 g) during an OGTT after 8–10 h of fasting.[16],[17]

Short comings

This test should not be performed in patients who fulfil the criteria for diabetes mellitus. These are (1) a fasting plasma glucose >7.0 mmol/L on two or more occasions or (2) clinical symptoms of diabetes, e.g., polydipsia, polyuria, ketonuria, and rapid weight loss with a random plasma glucose of >11.1 mmol/LThis test should not be performed in patients who are under physical stress, for example, postsurgery, trauma or infection or extreme psychological stress as these may give misleading resultsThis test should not be performed in patients with periodic hypokalaemic paralysis.

Fasting insulin

Fasting insulin level monitoring has long been seen to be the most practicable method for determining IR.[18] It has a strong link to IR. Fasting insulin levels and insulin action as determined by the clamp technique have been found to have a strong relationship. Because glucose levels fluctuate rapidly in the postprandial state, measuring IR using fasting insulin should be done after an overnight fast to avoid confounding the simultaneous measurement of insulin.

The limitation of the validity of HOMA-IR should be carefully considered in subjects with a lower body mass index, a lower beta cell function, and high fasting glucose levels such as lean type 2 diabetes mellitus with insulin secretory defects.

Glucose/insulin ratio

A number of studies have used the glucose/insulin (G/I) ratio as an indicator of IR.[19] In nondiabetics, it will be functionally similar to 1/(fasting insulin), as fasting glucose levels are all within normal limits, albeit it does not accurately reflect the physiology underlying the determinants of insulin sensitivity.[20] The fasting G/I ratio is an imprecise indicator of insulin sensitivity in theory.

The potential problems with using the fasting G/I ratio as a physiologically appropriate index of insulin sensitivity become apparent when fasting glucose levels are abnormal. This is easily illustrated by comparing a normal subject with an insulin-resistant nondiabetic subject and an insulin-resistant subject with type 2 diabetes, when a normal subject is compared with a nondiabetic insulin-resistant subject (whose fasting insulin level is elevated), simple indices of insulin sensitivity based on fasting values such as 1/insulin, QUICKI, and G/I are all decreased in the insulin-resistant subject when compared with the normal subject, just as expected. He/she fasting G/I ratio is a potentially flawed index of insulin sensitivity whose test characteristics are likely to be similar to 1/insulin in nondiabetic subjects. More robust and accurate simple indices of insulin sensitivity such as QUICKI and log[HOMA] would appear to have greater clinical utility.

Insulinogenic index

The insulinogenic index (IGI) is a commonly used b-cell function indicator. It is an insulin secretion index generated from the OGTT. Glucose is measured in milligrams per deciliter, but insulin is measured in microunits per milliliter.[21] With a more physiological way of glucose administration, the IGI can be used to quantify the degree of insulin production.

Fasting insulin resistance index

Duncan et al. developed the fasting IR index in pursuit of a separate marker, as the use of a glucose-insulin ratio may not be useful for estimating IR. Increased insulin production to restore a normal level of plasma glucose results in a long-term increase in insulin and, most likely, glucose.[22]

a 13C glucose breath test

Breath testing is based on the idea that a consumed substrate is digested and subsequently exhaled by the respiratory system as a detectable metabolite. For decades, breath testing has been employed in both research and therapeutic settings.[23] The C-methacetin breath test (MBT), which measures hepatic microsomal function (CYP1A2), is a laser-based technology that produces an infrared emission that matches the CO2 absorption spectrum exactly. When detecting CO2 using molecular correlation spectroscopy, MBT can detect fluctuations of <1/1000 in the 13CO2/12CO2 ratio.

The triglyceride and glucose index

The triglyceride and glucose index has recently gained popularity as a result of the readily available and low-cost biochemical markers required for its calculation. Fasting plasma glucose and fasting triglyceride levels are used to calculate it.[24]

  Conclusion and Implications 

Despite various methods and tools for calculating IR, prevalence of IR is still high, and there is no gold standard, cost-effective method or tool to determine the same.

To summarise, this article examines a range of approaches for assessing insulin sensitivity/resistance that are currently accessible. IR is becoming more widely assessed in clinical settings, necessitating the development of very simple indicators. Surrogate markers are a valuable tool for determining IR. These treatments range from complex, time-consuming, and invasive procedures to simple diagnostics requiring only a single fasting blood sample. The glucose clamp method has long been the gold standard for measuring insulin sensitivity directly. Surrogate markers for assessing IR could thus help to maximize the utilization of medicinal resources while reducing expenses and undesirable side effects.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 

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  [Figure 1]