Optimal GGT Levels: More Than a Liver Enzyme | Optimal DX Blog

GGT is much more than a liver enzyme, it’s a metabolic clue

Dicken Weatherby, N.D. and Beth Ellen DiLuglio, MS, RDN, LDN

Overview

GGT has historically been viewed as a liver enzyme and a clue to emerging hepatobiliary dysfunction. In this post, we present a wider view of GGT's role in identifying dysfunction and posit a new and updated optimal range.

Gamma-glutamyltransferase (GGT) is a glycoprotein enzyme found in most mammalian cells.

GGT assists in amino acid transfer and leukotriene conversion, but its primary function is the metabolism of the tripeptide antioxidant compound glutathione.[1] Glutathione is a major antioxidant as well as a key compound in detoxification pathways.

Glutathione is crucial to cellular health and is maintained at levels equal to those of glucose, potassium, and cholesterol. Glutathione not only directly scavenges free radicals, but it is able to regenerate antioxidant vitamins C and E.[2]

GGT is abundant in hepatocytes and is considered a “liver enzyme” as it becomes elevated in the blood when liver damage occurs. GGT is also a sensitive marker for gallbladder issues such as cholestasis, cholecystitis, cholangitis, and biliary obstruction.[3]

However, GGT is much more than a liver enzyme. It is considered a biomarker for metabolic and cardiovascular disorders including metabolic syndrome, diabetes, coronary artery disease (CAD), and stroke. Not surprisingly, it is associated with related risk factors including insulin resistance, obesity, hypertension, and fatty liver.[4]

GGT Recycles Glutathione

Oxidative stress, inflammation, and exposure to toxins (e.g., pesticides, mercury, cadmium, etc.) can deplete the reduced form of glutathione (GSH), contributing to mitochondrial and cellular dysfunction. An increased need will trigger the recycling of oxidized glutathione (GSSG) to provide cysteine for de novo synthesis of GSH, a reaction catalyzed by GGT. Provision of exogenous cysteine in the form of whey protein or supplemental N-acetylcysteine was found to reduce the need for glutathione recycling and decreased GGT levels by 25%.[5]

Serum GGT is useful as a marker of oxidative stress due to the inverse relationship between GGT activity and plasma glutathione. [6]

Elevated GGT is Observed in Many Disorders

Serum levels of GGT are used to monitor hepatic inflammation, biliary obstruction, and exposure to excess alcohol. However, it is increasingly recognized as a marker for other dysfunctions. GGT activity may be increased in:[7] [8] [9] [10]

• Alcohol excess, chronic alcohol intake
• All-cause mortality
• Arterial stiffness
• Atherosclerosis, plaque
• Biliary disease
• Cancer
• Cholestasis
• Chronic kidney disease (CKD)
• Congestive heart failure
• Cytomegalovirus infection
• Dementia
• Diabetes
• Epstein-Barr virus (mononucleosis)
• Environmental toxin exposure
• Fasting insulin
• Fractures
• Glutathione depletion
• Heart failure
• Inflammation, systemic
• Jaundice
• Liver disease, fatty liver, hepatic tumor or metastasis, viral hepatitis
• Obesity
• Medication use (e.g., furosemide, heparin, phenobarbital, phenytoin)
• Metabolic syndrome
• Oxidative stress
• Pancreatic cancer
• Periodontal disease
• Reye syndrome
• Smoking
• Vascular disease
• Men may have higher levels than women, and black populations may have higher levels than Caucasians
• Positive association of GGT with age, BMI, ferritin, glucose, lipids (triglycerides, total and LDL cholesterol), uric acid, waist circumference
• Inverse association of GGT with HDL cholesterol, lung function, physical activity

Serum GGT levels are associated with exposure to environmental toxins including heavy metals, polycyclic aromatic hydrocarbons, dioxins, and organochlorine pesticides.[11] This association is not surprising given GGT’s role in glutathione metabolism and detoxification of persistent organic pollutants. Loss of antioxidant protection along with inadequate detoxification can dramatically increase oxidative stress and the risk of disease.[12]

Since upregulation of GGT is proportional to toxin exposure, we must be sure to investigate all potential sources of contributing toxins including air, food, and water.

Monitoring GGT Levels

As glutathione is depleted, oxidative changes take place that affects lipids, proteins, and even nucleotides in the cell. These changes contribute to insulin resistance and set off a chain of events that can lead to diabetes and other metabolic disorders. The MESA cohort study confirmed that those in the lowest quintile for GGT of less than 24.5 U/L (the lowest cut-off used) had the lowest risk of metabolic disease with significantly lower fasting glucose (85 mg/dL), fasting insulin (3.8 uU/L), LDL cholesterol (114.1 mg/dL), and triglycerides (94 mg/dL), and the highest HDL cholesterol (56.7 mg/dL).[13]

A follow-up study of 22,931 Korean men with no insulin resistance at baseline revealed that GGT levels above 18 U/L were significantly associated with increased risk of insulin resistance, hypertension, and alcohol use, as well as elevations in fasting glucose, insulin, total and LDL cholesterol, triglycerides, AST, and ALT.[14]

Elevated GGT and insulin resistance significantly increase the risk and incidence of non-alcoholic fatty liver disease (NAFLD) so a full clinical workup would be prudent.[15]

A prospective cohort study of 13,435 Korean men found that levels of GGT above 17 U/L at baseline were associated with a progressively increased risk of prehypertension. Levels above 17 U/L were also associated with increased BMI, alcohol intake, triglycerides, hs-CRP, fasting glucose and insulin, and total and LDL cholesterol.[16]  

One study of CAD patients observed progressively increasing GGT with increased artery obstruction: [17]

In a cross-sectional study of 14,439 Korean subjects without CAD, coronary artery calcification (CAC) was lowest in men with GGT of 21 U/L or less, and women with a GGT of 10 U/L or less. The risk of CAC increased progressively as GGT increased. Levels of fasting glucose, triglycerides, and total and LDL cholesterol increased progressively in both groups as well.[18]

A small study of 138 subjects in Turkey revealed that subjects with coronary plaques had a mean GGT of 35.7 U/L while the average GGT in those without plaques was 19.6 U/L. Plaques were also significantly associated with diabetes, hemoglobin A1C, hs-CRP, hyperlipidemia, hypertension, and uric acid.[19]

The Apolipoprotein Mortality Risk (AMORIS) cohort study of 545,460 individuals demonstrated a positive association between GGT of 18 U/L or greater with progressively increased risk of cancer, especially breast, prostate, liver, respiratory, urinary, digestive tract cancers.[20]

A review of the Framingham Offspring Study revealed that morbidity and mortality were two-fold greater in those with baseline GGT levels above 16 U/L for men and 9 U/L for women.[21]

Elevations in GGT are seen with the same dietary patterns associated with many chronic diseases, including excess alcohol intake, meat intake, and lack of plant-based foods. When looking at the association between GGT and dietary factors, The Coronary Artery Risk Development in Young Adults (CARDIA) observed: [22]

• Positive associations between GGT and meats, heme iron, and alcohol.
• Inverse associations between GGT and plant-based foods (fruit, whole grains, nuts) with a weak inverse association with poultry, fish, coffee, and sucrose
• Inverse associations with nutrients consumed in food form (beta-carotene, vitamin C, fiber, folate) but a positive associate with GGT when those nutrients were consumed in isolated supplement form.

GGT's Association with Other Biomarkers

In the prospective Kerman Coronary Artery Disease Risk Study (KERCADRS), those in the first quartile of GGT (less than 13 U/L) had significantly higher HDL, and significantly lower: [23]

• Diastolic and systolic blood pressure mean 76.9/114.4
• Fasting glucose mean 87 mg/dL  
• Incidence of metabolic syndrome 26%
• Impaired glucose tolerance 5%
• Triglycerides mean 97 mg/dL      
• Waist circumference   mean 31.8 inches (80.7 cm)
• Each of these parameters increased as GGT increased

Alkaline phosphatase

Levels of GGT often parallel those of alkaline phosphatase in hepatobiliary disease. However, in bone-related diseases, alkaline phosphatase will be elevated while GGT will not.[24]

In some cases, a significantly greater rise in alkaline phosphatase (e.g., 2.5-fold increase above standard range to ~130 IU/L) may help differentiate the presence of common bile duct stones from acute cholecystitis where there may not be a significant difference in GGT between the two conditions.[25]

In subjects with Coronary Heart Disease (CHD), a GGT greater than the median of 36.2 U/L was strongly correlated with all-cause mortality while alkaline phosphatase was greater than its median of 69.3 U/L did not correlate.[26]

In pre-dialysis patients with stage 4-5 chronic kidney disease, GGT above 36 U/L was associated with increased mortality, more comorbidities, and higher ferritin, C-reactive protein, uric acid, triglycerides, and ALT levels. Though alkaline phosphatase above 120 U/L was insignificantly associated with mortality, the risk increased when GGT was also elevated above 36 U/L.[27]

Ferritin

A positive association is observed between GGT and ferritin[28] with an apparent synergistic association between these two markers and metabolic syndrome.[29]

A study of 1024 individuals revealed that elevations of GGT and serum ferritin synergistically increased the risk of chronic kidney disease. The group with both GGT and ferritin in the 4th quartile had increased risk of CKD, increased alcohol intake, higher BMI, and increasing prevalence of metabolic syndrome, diabetes, hypertension, hypertriglyceridemia, and elevated malondialdehyde (an oxidative stress marker).[30]

• Mean values in Quartile 1 include GGT of 13 U/L for men and 9 U/L for women, with serum ferritin of 130.2 umol/L for men and 43.4 umol/L for women.
• Mean values in Quartile 4 include GGT of 105.5 U/L for men and 50 U/L for women, with serum ferritin of 270.6 umol/L for men and 104.3 umol/L for women

HDL

High-density lipoprotein (HDL) serves an important role in disease prevention due to its antioxidant, anti-inflammatory, and anti-thrombotic properties. Reductions in HDL cholesterol reflect an increase in metabolic dysfunction including an increased risk of NAFLD. A cross-sectional study investigated an association between low HDL-C and elevated GGT. Subjects with NAFLD had higher GGT to HDL-C ratios than those without NAFLD. Researchers observed a 0.3% increased prevalence of NAFLD for every 1 unit increase in GGT: HDL-C ratio.[31]

In the highest quartile, the prevalence of NAFLD is expected to be 6.362 times higher than for those in the lowest quartile. For metabolic syndrome, the prevalence was expected to be 3.968 times higher in the 4th versus the 1st quartile. Those with NAFLD had a mean GGT of 33 U/L versus 18 U/L in those without NAFLD.

Guilt By Association?

Is elevated GGT a beneficial response to oxidative stress and metabolic dysfunction or is it pathological in and of itself?

Elevations in GGT occur in the face of oxidative stress as it facilitates the metabolism of glutathione as well as glutathionylated xenobiotics. However, researchers postulate that it may become a pro-oxidant, particularly in the presence of iron or copper. These metal-based nutrients may be released from red blood cells during GGT elevation, creating a perpetual oxidative chain reaction.[32] Research suggests further investigation into this apparent conundrum.[33]

It appears that an increase in GGT reflects increased production of glutathione and maintenance of intracellular GSH in response to oxidative stress and not a singular cause of oxidative stress.

Since the loss of red blood cell membrane integrity is a concern during GGT elevation, it should be noted that research suggests it can be improved with the incorporation of heptadecanoic acid, a C:17 saturated fatty acid. Human research indicates that this fatty acid can be protective against inflammation, metabolic syndrome, and type 2 diabetes. An interesting study of dolphins with metabolic syndrome indicated that increased intake of heptadecanoic acid was associated with a significant reduction in serum ferritin and a return to normal serum glucose, insulin, and triglycerides. Whole fat bovine milk, shrimp, and some fish are notable sources of heptadecanoic acid. Butter is an excellent source, containing ten times more than any other food.[34]

A Healthy Lifestyle Can Help Support Glutathione Metabolism and Tame GGT

Perhaps we should not “shoot the messenger” but instead focus on the causes of oxidative stress and take definitive steps to decrease it.

Simple pertinent steps include a healthy plant-based diet based on whole foods and an abundance of fresh vegetables, fruits, and nuts that provide important exogenous antioxidants. The addition of whey can provide cysteine for the rate-limiting step of producing endogenous glutathione.

It is equally important to reduce exposure to air pollution and toxic chemicals, heavy metals, and pesticides that can cause oxidative stress and cellular dysfunction.

For more information on Oxidative Stress please review the ODX Series on Oxidative Stress

Reference Ranges

Reference ranges for GGT may be influenced by [35]

• Childbirth
• Exercise
• Gender (males tend to have higher levels than females until menopause)
• Oral contraceptive use
• Race

Researchers recognize that levels of GGT at the upper end of the standard reference range warrant further evaluation. It is especially important to investigate in smokers, significant alcohol intake, increased BMI, and medication use.[36]

In the event of elevated GGT above the optimal range, further assessment and screening for metabolic syndrome, type 2 diabetes, heart disease, non-alcoholic fatty liver disease, and other comorbidities would be prudent.

Standard Reference Ranges

Optimal ranges for GGT:

• Above 16.5 U/L was associated with metabolic syndrome and above 20.5 U/L was associated with impaired glucose tolerance.[41]
• 9-35 U/L was associated with a progressively increased risk of Type 2 diabetes.[42]
• GGT above 18 U/L was associated with insulin resistance, prehypertension, and cancer.[43] [44] [45]
• GGT of less than 24.5 U/L (lowest quintile defined, not further categorized) had the lowest risk of metabolic disease with significantly lower fasting glucose (85 mg/dL), fasting insulin (3.8 uU/L), LDL cholesterol (114.1 mg/dL), and triglycerides (94 mg/dL), and the highest HDL cholesterol (56.7 mg/dL).[46]

Optimal Takeaways

• GGT plays a crucial role in cellular defense and maintenance of intracellular glutathione. Elevations reflect the presence of significant oxidative stress and stressors.
• Elevated GGT is recognized as a predictor of alcohol abuse, coronary artery disease, stroke, hypertension, metabolic syndrome, and type 2 diabetes.[47]
• GGT levels above 17 IU/L should trigger an evaluation of alcohol intake, toxin exposure, oxidative stress, fatty liver, insulin resistance, metabolic syndrome, and cardiovascular risk.
• Nutrition and lifestyle recommendations to reduce oxidative stress and decrease GGT levels includes: [48]
  • A nutrient-dense plant-based diet limited in meat, heme iron, and alcohol
  • Regular physical activity
  • Healthy weight maintenance using balanced macronutrients, an abundance of micronutrients and antioxidants, adequate hydration, and regular structured exercise
  • Avoidance of pollutants, toxins, pesticides, heavy metals, and other oxidative stress triggers
• Increased production of glutathione can reduce the need for GGT-mediated glutathione recycling. Production may be increased with the consumption of whey protein, N-acetylcysteine, 2-3 ounces of almonds, 500 mL of alcohol-free beer, and with meditation.[49]
• Consumption of heptadecanoic acid can support red blood cell membrane integrity and reduce the consequences of oxidative stress. Butter and whole fat dairy products are best sources, organic is recommended.
• GGT and related biomarkers should be repeated 2-3 months following intervention to assess progress.

Additional references[50] [51] [52] [53] [54] [55] 

Research

[1] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[2] Pizzorno, Joseph. “Glutathione!.” Integrative medicine (Encinitas, Calif.) vol. 13,1 (2014): 8-12.

[3] Pagana, Kathleen Deska; Pagana, Timothy J.; Pagana, Theresa N. Mosby's Diagnostic and Laboratory Test Reference - E-Book (Kindle Locations 10506-10508). Elsevier Health Sciences. Kindle Edition.

[4] Yousefzadeh, Gholamreza et al. “Role of gamma-glutamyl transferase (GGT) in diagnosis of impaired glucose tolerance and metabolic syndrome: a prospective cohort research from the Kerman Coronary Artery Disease Risk Study (KERCADRS).” Diabetes & metabolic syndrome vol. 6,4 (2012): 190-4. doi:10.1016/j.dsx.2012.08.013 

[5] Pizzorno, Joseph. “Glutathione!.” Integrative medicine (Encinitas, Calif.) vol. 13,1 (2014): 8-12. 

[6] Bradley, Ryan et al. “Associations between total serum GGT activity and metabolic risk: MESA.” Biomarkers in medicine vol. 7,5 (2013): 709-21. doi:10.2217/bmm.13.71 

[7] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[8] Pagana, Kathleen Deska; Pagana, Timothy J.; Pagana, Theresa N. Mosby's Diagnostic and Laboratory Test Reference - E-Book (Kindle Locations 10506-10508). Elsevier Health Sciences. Kindle Edition.

[9] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[10] Feng, Guofang et al. “Association between ratio of γ-glutamyl transpeptidase to high-density lipoprotein cholesterol and prevalence of nonalcoholic fatty liver disease and metabolic syndrome: a cross-sectional study.” Annals of translational medicine vol. 8,10 (2020): 634. doi:10.21037/atm-19-4516 

[11] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[12] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[13] Bradley, Ryan et al. “Associations between total serum GGT activity and metabolic risk: MESA.” Biomarkers in medicine vol. 7,5 (2013): 709-21. doi:10.2217/bmm.13.71 

[14] Ryoo, J H et al. “Clinical association between serum γ-glutamyltransferase levels and the development of insulin resistance in Korean men: a 5-year follow-up study.” Diabetic medicine : a journal of the British Diabetic Association vol. 31,4 (2014): 455-61. doi:10.1111/dme.12315 

[15] Hossain, Israt Ara et al. “Gamma glutamyl transferase is an independent determinant for the association of insulin resistance with nonalcoholic fatty liver disease in Bangladeshi adults: Association of GGT and HOMA-IR with NAFLD.” Diabetes & metabolic syndrome vol. 10,1 Suppl 1 (2016): S25-9. doi:10.1016/j.dsx.2015.09.005 

[16] Chun, Hyejin et al. “Association of serum γ-glutamyltransferase level and incident prehypertension in Korean men.” Journal of Korean medical science vol. 28,11 (2013): 1603-8. doi:10.3346/jkms.2013.28.11.1603 

[17] Arasteh, Siavash et al. “Serum level of gamma-glutamyl transferase as a biomarker for predicting stenosis severity in patients with coronary artery disease.” Indian heart journal vol. 70,6 (2018): 788-792. doi:10.1016/j.ihj.2017.11.017 

[18] Lee, Woncheol et al. “Association of coronary artery calcification and serum gamma-glutamyl transferase in Korean.” Atherosclerosis vol. 226,1 (2013): 269-74. doi:10.1016/j.atherosclerosis.2012.10.059 

[19] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[20] Van Hemelrijck, Mieke et al. “Gamma-glutamyltransferase and risk of cancer in a cohort of 545,460 persons - the Swedish AMORIS study.” European journal of cancer (Oxford, England : 1990) vol. 47,13 (2011): 2033-41. doi:10.1016/j.ejca.2011.03.010 

[21] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[22] Lee, Duk-Hee et al. “Association between serum gamma-glutamyltransferase and dietary factors: the Coronary Artery Risk Development in Young Adults (CARDIA) Study.” The American journal of clinical nutrition vol. 79,4 (2004): 600-5. doi:10.1093/ajcn/79.4.600 

[23] Yousefzadeh, Gholamreza et al. “Role of gamma-glutamyl transferase (GGT) in diagnosis of impaired glucose tolerance and metabolic syndrome: a prospective cohort research from the Kerman Coronary Artery Disease Risk Study (KERCADRS).” Diabetes & metabolic syndrome vol. 6,4 (2012): 190-4. doi:10.1016/j.dsx.2012.08.013 

[24] Pagana, Kathleen Deska; Pagana, Timothy J.; Pagana, Theresa N. Mosby's Diagnostic and Laboratory Test Reference - E-Book (Kindle Locations 10506-10508). Elsevier Health Sciences. Kindle Edition.

[25] Thapa, P B et al. “Serum gamma glutamyl transferase and alkaline phosphatase in acute cholecystitis.” Journal of Nepal Health Research Council vol. 8,2 (2010): 78-81. 

[26] Ndrepepa, G et al. “A comparison of gamma-glutamyl transferase and alkaline phosphatase as prognostic markers in patients with coronary heart disease.” Nutrition, metabolism, and cardiovascular diseases : NMCD vol. 28,1 (2018): 64-70. doi:10.1016/j.numecd.2017.09.005 

[27] Caravaca-Fontán, Fernando et al. “High levels of both serum gamma-glutamyl transferase and alkaline phosphatase are independent preictors of mortality in patients with stage 4-5 chronic kidney disease.” Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia vol. 37,3 (2017): 267-275. doi:10.1016/j.nefro.2016.11.010 

[28] Lee, Duk-Hee et al. “Association between serum gamma-glutamyltransferase and dietary factors: the Coronary Artery Risk Development in Young Adults (CARDIA) Study.” The American journal of clinical nutrition vol. 79,4 (2004): 600-5. doi:10.1093/ajcn/79.4.600 

[29] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[30] Chen, Tao et al. “Serum Gamma-Glutamyl Transferase and Ferritin Synergistically Associated with the Rate of Chronic Kidney Disease.” Disease markers vol. 2017 (2017): 9765259. doi:10.1155/2017/9765259 

[31] Feng, Guofang et al. “Association between ratio of γ-glutamyl transpeptidase to high-density lipoprotein cholesterol and prevalence of nonalcoholic fatty liver disease and metabolic syndrome: a cross-sectional study.” Annals of translational medicine vol. 8,10 (2020): 634. doi:10.21037/atm-19-4516 

[32] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[33] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[34] Koenig, Gerald, and` Stephanie Seneff. “Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk.” Disease markers vol. 2015 (2015): 818570. doi:10.1155/2015/818570 

[35] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[36] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[37] Quest Diagnostics. GGT. 

[38] Labcorp. GGT. 

[39] Pagana, Kathleen Deska; Pagana, Timothy J.; Pagana, Theresa N. Mosby's Diagnostic and Laboratory Test Reference - E-Book (Kindle Locations 10506-10508). Elsevier Health Sciences. Kindle Edition.

[40] Lee, Duk-Hee et al. “Association between serum gamma-glutamyltransferase and dietary factors: the Coronary Artery Risk Development in Young Adults (CARDIA) Study.” The American journal of clinical nutrition vol. 79,4 (2004): 600-5. doi:10.1093/ajcn/79.4.600 

[41] Yousefzadeh, Gholamreza et al. “Role of gamma-glutamyl transferase (GGT) in diagnosis of impaired glucose tolerance and metabolic syndrome: a prospective cohort research from the Kerman Coronary Artery Disease Risk Study (KERCADRS).” Diabetes & metabolic syndrome vol. 6,4 (2012): 190-4. doi:10.1016/j.dsx.2012.08.013

[42] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[43] Ryoo, J H et al. “Clinical association between serum γ-glutamyltransferase levels and the development of insulin resistance in Korean men: a 5-year follow-up study.” Diabetic medicine : a journal of the British Diabetic Association vol. 31,4 (2014): 455-61. doi:10.1111/dme.12315 

[44] Chun, Hyejin et al. “Association of serum γ-glutamyltransferase level and incident prehypertension in Korean men.” Journal of Korean medical science vol. 28,11 (2013): 1603-8. doi:10.3346/jkms.2013.28.11.1603 

[45] Van Hemelrijck, Mieke et al. “Gamma-glutamyltransferase and risk of cancer in a cohort of 545,460 persons - the Swedish AMORIS study.” European journal of cancer (Oxford, England : 1990) vol. 47,13 (2011): 2033-41. doi:10.1016/j.ejca.2011.03.010 

[46] Bradley, Ryan et al. “Associations between total serum GGT activity and metabolic risk: MESA.” Biomarkers in medicine vol. 7,5 (2013): 709-21. doi:10.2217/bmm.13.71 

[47] Ryoo, J H et al. “Clinical association between serum γ-glutamyltransferase levels and the development of insulin resistance in Korean men: a 5-year follow-up study.” Diabetic medicine : a journal of the British Diabetic Association vol. 31,4 (2014): 455-61. doi:10.1111/dme.12315 

[48] Kunutsor, Setor K. “Gamma-glutamyltransferase-friend or foe within?.” Liver international : official journal of the International Association for the Study of the Liver vol. 36,12 (2016): 1723-1734. doi:10.1111/liv.13221 

[49] Pizzorno, Joseph. “Glutathione!.” Integrative medicine (Encinitas, Calif.) vol. 13,1 (2014): 8-12. 

[50] Onat, Altan et al. “Serum γ-glutamyltransferase: independent predictor of risk of diabetes, hypertension, metabolic syndrome, and coronary disease.” Obesity (Silver Spring, Md.) vol. 20,4 (2012): 842-8. doi:10.1038/oby.2011.136 

[51] Neuman, Manuela G et al. “Gamma glutamyl transferase - an underestimated marker for cardiovascular disease and the metabolic syndrome.” Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques vol. 23,1 (2020): 65-74. doi:10.18433/jpps30923 

[52] Ndrepepa, Gjin et al. “Gamma-glutamyl transferase and prognosis in patients with coronary artery disease.” Clinica chimica acta; international journal of clinical chemistry vol. 452 (2016): 155-60. doi:10.1016/j.cca.2015.11.013 

[53] Ndrepepa, Gjin et al. “Gamma-glutamyl transferase and the risk of atherosclerosis and coronary heart disease.” Clinica chimica acta; international journal of clinical chemistry vol. 476 (2018): 130-138. doi:10.1016/j.cca.2017.11.026 

[54] Ndrepepa, Gjin, and Adnan Kastrati. “Gamma-glutamyl transferase and cardiovascular disease.” Annals of translational medicine vol. 4,24 (2016): 481. doi:10.21037/atm.2016.12.27 

[55] Bharani, Vani, et al. "Evaluation of gamma glutamyl transferase as a marker of cardiovascular risk, in 200 angiographically proven coronary artery disease patients." Indian heart journal 69.3 (2017): 325-327.