Why is fasting required for this panel?

Glucose, insulin, and triglycerides rise substantially after meals, so a 10–12 hour overnight fast is essential to obtain baseline values that can be compared to diagnostic and risk-stratification thresholds.

What does an elevated HOMA-IR indicate?

Elevated HOMA-IR (generally >2.5) indicates insulin resistance — the body requires higher insulin levels to maintain normal glucose. It is an early marker of metabolic dysfunction, often appearing before glucose rises into the prediabetic range.

Is high-sensitivity CRP the same as regular CRP?

High-sensitivity CRP uses an assay capable of detecting low concentrations relevant to cardiovascular risk stratification, whereas standard CRP is used to detect acute inflammation from infection or injury. The hs-CRP range for cardiovascular risk is 3 mg/L.

What does elevated homocysteine mean?

Elevated homocysteine (>15 µmol/L) suggests folate or B12 deficiency, MTHFR gene polymorphisms, or chronic kidney disease. It is an independent marker of cardiovascular and thrombotic risk, though B-vitamin supplementation lowers homocysteine without proven cardiovascular benefit.

Can this panel diagnose diabetes?

Yes. Fasting glucose ≥7.0 mmol/L or HbA1c ≥6.5% meets diagnostic criteria for diabetes mellitus, though guidelines recommend confirmation with a repeat test in asymptomatic individuals.

Should patients take medications before the test?

Most maintenance medications can be taken after the draw, but patients should follow their prescriber's instructions. Insulin and glucose-lowering agents may be adjusted for the fasting state; clarify with the ordering practitioner.

How long until results are available?

Results are typically available in 5–7 business days from specimen receipt at DHA Laboratory, though turnaround may be longer during holidays or if additional testing is required.

Does this panel replace a standard lipid panel?

It includes a full lipid panel (total cholesterol, LDL-C, HDL-C, triglycerides) as well as markers of insulin resistance and inflammation, so it provides a more comprehensive cardiometabolic assessment than a standalone lipid test.

BML-MET-019metabolic diabetesUSA

Advanced Metabolic Panel Plus

The Advanced Metabolic Panel Plus measures fasting glucose, HbA1c, insulin, HOMA-IR, lipids, kidney function, uric acid, hs-CRP, and homocysteine in a single profile. It provides granular assessment of insulin resistance, cardiometabolic risk, and systemic inflammation, enabling early detection and monitoring of prediabetes, metabolic syndrome, and cardiovascular disease.

Biomarkers

Blood (plasma)

Sample

5–7 business days

Turnaround

Yes — 10–12 hours

Fasting

What is the AMP Plus test?

The Advanced Metabolic Panel Plus combines core markers of glucose metabolism, insulin resistance, lipid health, kidney function, and systemic inflammation in a single comprehensive profile. It is designed for practitioners who want a granular view of metabolic and cardiometabolic risk beyond the traditional basic metabolic panel, capturing insulin dynamics, chronic low-grade inflammation, and one-carbon metabolism. This panel is particularly suited to early detection and monitoring of metabolic syndrome, prediabetes, insulin resistance, and cardiovascular risk in patients with normal or borderline routine tests. By including HOMA-IR, fasting insulin, hs-CRP, and homocysteine alongside standard metabolic markers, it enables intervention at a stage when lifestyle and nutraceutical strategies may still reverse or forestall progression to overt diabetes and atherosclerotic disease.

What does the AMP Plus test measure?

FPG(Fasting Plasma Glucose)

Range: 3.9–5.5 mmol/L (70–99 mg/dL)Optimal: Functional practitioners often target 4.4–5.0 mmol/L (80–90 mg/dL) for metabolic optimisation, though evidence for these tighter thresholds is less robust than established diagnostic cut-offs.mmol/L / mg/dL

Glucose is the primary metabolic fuel for all tissues and is tightly regulated by insulin secretion, hepatic production, and peripheral uptake. Fasting plasma glucose reflects the balance between endogenous glucose output and basal insulin action in the absence of exogenous carbohydrate load.

Fasting glucose is a cornerstone of diabetes screening and diagnosis. Values ≥7.0 mmol/L meet the diagnostic threshold for diabetes mellitus, while 5.6–6.9 mmol/L define prediabetes. Persistently elevated fasting glucose signals impaired insulin secretion, increased hepatic gluconeogenesis, or reduced peripheral glucose uptake.

HbA1c(Glycated Haemoglobin A1c)

Range: <5.7% (39 mmol/mol)Optimal: Most guidelines recommend <7% as a treatment target for adults with established diabetes; tighter targets (<6.5%) may be appropriate for selected individuals, while higher targets (7.5–8%) suit older or frailer patients.% of total Hb / mmol/mol

HbA1c is formed by the non-enzymatic glycation of haemoglobin over the lifespan of the red cell, approximately 120 days. It integrates ambient glucose exposure and provides a time-averaged glycaemic index independent of daily fluctuations.

HbA1c is used both diagnostically (≥6.5% for diabetes, 5.7–6.4% for prediabetes) and to monitor long-term glycaemic control in established diabetes. It is less influenced by acute stress, fasting state, or single meals, making it complementary to fasting and postprandial glucose measurements.

Insulin(Fasting Insulin)

Range: Approximately 18–173 pmol/L (3–25 µU/mL), method- and population-dependentOptimal: Functional-medicine practitioners often favour fasting insulin <60 pmol/L (<10 µU/mL) as a marker of insulin sensitivity, though this threshold is not universally accepted in mainstream endocrinology.pmol/L / µU/mL

Insulin is secreted by pancreatic beta cells in response to glucose and other nutrients. Fasting insulin reflects basal secretion and the degree of insulin resistance — when peripheral tissues resist insulin's actions, the pancreas compensates by increasing output, driving fasting insulin upward.

Elevated fasting insulin is an early marker of insulin resistance, often appearing years before glucose rises into the prediabetic range. It is used to calculate HOMA-IR and other insulin-resistance indices, to assess beta-cell reserve, and to stratify metabolic risk in patients with normal glucose.

HOMA-IR(Homeostatic Model Assessment of Insulin Resistance)

Range: <2.0 (insulin-sensitive), >2.5 (insulin-resistant); population-specificOptimal: Optimal thresholds vary by ethnicity and age; <1.5 is often considered highly insulin-sensitive, while >2.5 indicates clinically significant resistance.dimensionless

HOMA-IR is derived from fasting glucose and fasting insulin using the formula [fasting insulin (µU/mL) × fasting glucose (mmol/L)] / 22.5. It estimates steady-state beta-cell function and insulin resistance from a single fasting sample and correlates well with hyperinsulinaemic-euglycaemic clamp measurements.

HOMA-IR provides a practical, low-cost surrogate for insulin resistance in clinical and research settings. Rising HOMA-IR predicts progression to type 2 diabetes and is used to guide early lifestyle and pharmacological interventions in metabolically at-risk individuals.

TG(Fasting Triglycerides)

Range: <1.7 mmol/L (150 mg/dL)Optimal: Many lipid guidelines favour <1.0 mmol/L (90 mg/dL) for optimal cardiometabolic health, though this target is not universally adopted.mmol/L / mg/dL

Triglycerides are the predominant form of circulating fat, carried in very-low-density lipoproteins and chylomicrons. Fasting triglyceride concentration reflects hepatic VLDL secretion, which is driven by carbohydrate and alcohol intake, insulin resistance, and genetic factors.

Elevated triglycerides are a component of metabolic syndrome, signal insulin resistance and hepatic steatosis, and contribute to cardiovascular risk. Very high triglycerides (>5.6 mmol/L) raise the risk of acute pancreatitis.

HDL-C(High-Density Lipoprotein Cholesterol)

Range: >1.0 mmol/L (40 mg/dL) in men, >1.3 mmol/L (50 mg/dL) in womenOptimal: Optimal HDL-C is generally considered >1.5 mmol/L (60 mg/dL), though interventions that raise HDL-C do not consistently reduce cardiovascular events, suggesting that HDL function may matter more than concentration.mmol/L / mg/dL

HDL particles transport cholesterol from peripheral tissues to the liver for excretion (reverse cholesterol transport) and carry anti-inflammatory and antioxidant enzymes. HDL-C concentration is inversely associated with cardiovascular risk in population studies.

Low HDL-C is a metabolic-syndrome criterion and an independent cardiovascular risk factor. It is tightly linked to insulin resistance, obesity, and sedentary behaviour. HDL-C should be interpreted alongside triglycerides and apolipoprotein B for comprehensive lipid assessment.

LDL-C(Low-Density Lipoprotein Cholesterol (calculated))

Range: <3.0 mmol/L (115 mg/dL), risk-stratified targets lowerOptimal: Cardiovascular guidelines vary by region, but most recommend <1.8 mmol/L (70 mg/dL) for secondary prevention and <2.6 mmol/L (100 mg/dL) for moderate-risk primary prevention.mmol/L / mg/dL

LDL-C represents the cholesterol carried within LDL particles and is typically calculated from total cholesterol, HDL-C, and triglycerides using the Friedewald or Martin-Hopkins equations. LDL delivers cholesterol to peripheral tissues and is the principal atherogenic lipoprotein.

LDL-C is the primary target of lipid-lowering therapy in cardiovascular disease prevention. Guidelines stratify LDL-C targets by absolute cardiovascular risk — from <1.8 mmol/L in very-high-risk individuals to less aggressive targets in low-risk primary prevention.

TC(Total Cholesterol)

Range: <5.2 mmol/L (200 mg/dL)Optimal: Population targets vary; <5.0 mmol/L is a common public-health recommendation, though optimal levels depend on HDL-C and LDL-C distribution.mmol/L / mg/dL

Total cholesterol is the sum of cholesterol carried in all lipoprotein classes — LDL, HDL, and VLDL. It is an accessible screening measure but does not distinguish atherogenic from protective particles.

Total cholesterol is a standard component of lipid screening and cardiovascular risk assessment. Elevated total cholesterol prompts further lipid fractionation and risk stratification; however, it is less useful than LDL-C or non-HDL-C for guiding therapy.

Cr(Serum Creatinine)

Range: Approximately 60–110 µmol/L (0.7–1.2 mg/dL), sex- and age-dependentOptimal: Optimal creatinine is context-dependent — lower values in individuals with low muscle mass do not reflect superior kidney function, and mildly elevated creatinine in muscular individuals may be physiological.µmol/L / mg/dL

Creatinine is a breakdown product of muscle creatine phosphate, produced at a relatively constant rate and filtered by the glomeruli with minimal tubular reabsorption. Serum creatinine is therefore an indirect marker of glomerular filtration rate.

Creatinine is the cornerstone of kidney-function assessment, used to estimate GFR and stage chronic kidney disease. Rising creatinine signals declining filtration; it also informs dosing of renally cleared medications and contrast-agent decisions.

eGFR(Estimated Glomerular Filtration Rate)

Range: ≥90 mL/min/1.73 m²Optimal: Normal eGFR is age-dependent; mild declines occur with ageing, so a value of 60–89 in an older adult without other kidney markers may be physiological rather than pathological.mL/min/1.73 m²

eGFR is calculated from serum creatinine, age, sex, and race (though race coefficients are being re-evaluated) using equations such as CKD-EPI. It estimates the volume of plasma filtered by the kidneys per unit time, adjusted for body surface area.

eGFR is the primary tool for staging chronic kidney disease (CKD) and assessing kidney reserve. Values <60 mL/min/1.73 m² for more than three months define CKD stage 3 or worse, prompting specialist referral, medication review, and cardiovascular risk management.

UA(Serum Uric Acid)

Range: Approximately 150–420 µmol/L (2.5–7.0 mg/dL), sex-dependentOptimal: Some evidence suggests maintaining uric acid <360 µmol/L (6 mg/dL) to reduce gout flares and potentially to mitigate cardiovascular and renal risk, though the latter remains contested.µmol/L / mg/dL

Uric acid is the terminal oxidation product of purine metabolism, produced endogenously and from dietary purines, and excreted predominantly via the kidneys. Hyperuricaemia results from increased production, decreased renal excretion, or both.

Elevated uric acid is the biochemical hallmark of gout and is associated with insulin resistance, hypertension, metabolic syndrome, and chronic kidney disease. Very high levels (>540 µmol/L, 9 mg/dL) sharply increase the risk of gouty arthritis and urate nephropathy.

hs-CRP(High-Sensitivity C-Reactive Protein)

Range: <3.0 mg/L; cardiovascular risk strata: <1 low, 1–3 moderate, >3 highOptimal: For cardiovascular risk stratification, <1 mg/L is considered low risk; functional practitioners often target <0.5 mg/L, though trial evidence for intervention thresholds is limited.mg/L

C-reactive protein is an acute-phase reactant synthesised by the liver in response to interleukin-6 and other inflammatory cytokines. High-sensitivity assays detect low-grade chronic inflammation associated with metabolic and vascular disease, distinct from the acute elevations seen in infection or trauma.

hs-CRP is used to refine cardiovascular risk prediction in primary prevention, particularly in individuals at intermediate risk by traditional scores. Persistently elevated hs-CRP is associated with metabolic syndrome, insulin resistance, and atherosclerotic progression; acute elevations suggest intercurrent illness and warrant repeat testing.

Hcy(Plasma Homocysteine)

Range: 5–15 µmol/LOptimal: Many functional protocols target homocysteine <10 µmol/L, though the clinical benefit of such tight targets is uncertain.µmol/L

Homocysteine is a sulphur-containing amino acid derived from methionine, metabolised via remethylation (requiring folate and B12) and transsulphuration (requiring B6). Elevated homocysteine results from genetic variants (MTHFR polymorphisms), vitamin deficiencies, or renal impairment.

Hyperhomocysteinaemia is an independent marker of cardiovascular and thrombotic risk and a sensitive indicator of folate and B12 status. It is also elevated in chronic kidney disease and in patients on methotrexate or certain antiepileptics. Supplementation with B vitamins lowers homocysteine but has not consistently reduced cardiovascular events in trials.

Why is the AMP Plus test ordered?

Patients with a family history of type 2 diabetes, cardiovascular disease, or metabolic syndrome in whom routine screening is normal but clinical suspicion of insulin resistance remains
Overweight or obese individuals with central adiposity, fatty liver on imaging, or elevated liver enzymes suggestive of metabolic dysfunction-associated steatotic liver disease
Adults with borderline fasting glucose or HbA1c who require detailed insulin assessment to guide early intervention
Patients with dyslipidaemia — elevated triglycerides, low HDL-C, or small dense LDL — in whom atherogenic dyslipidaemia and insulin resistance are suspected
Individuals undergoing optimisation for longevity, performance, or weight loss who seek a baseline metabolic and inflammatory profile to track progress
Patients with hypertension, polycystic ovary syndrome, or non-alcoholic fatty liver disease, all of which cluster with insulin resistance
Follow-up monitoring of lifestyle, pharmacological, or nutraceutical interventions targeting metabolic health, particularly when insulin resistance or inflammation are treatment targets
Assessment of cardiovascular risk in intermediate-risk individuals for whom hs-CRP and advanced lipid markers refine statin and aspirin decisions

Sample collection and turnaround

Sample type

Blood (plasma)

Fasting required

Yes — 10–12 hours

Collection method

Venipuncture at patient service centre

Turnaround

5–7 business days

Collection notes

Phlebotomy via LabCorp patient service centres on behalf of DHA Laboratory. A 10–12 hour overnight fast (water permitted) is required for valid glucose, insulin, and lipid results. Advise patients to avoid strenuous exercise, alcohol, and high-fat meals the evening before, and to take medications after the draw unless otherwise directed. Plasma samples must be separated promptly and refrigerated; delayed processing can lower glucose and affect hs-CRP.

Specimen requirements

Minimum 5 mL plasma (typically collected in EDTA or sodium fluoride tubes depending on analyte). Separate plasma within 30 minutes of collection. Insulin and glucose samples are particularly time-sensitive.

What can affect AMP Plus results?

elevatesNon-fasting state

Glucose, insulin, and triglycerides rise postprandially, invalidating their interpretation as fasting markers. A 10–12 hour fast is required.

elevatesAcute illness, infection, or surgical stress

Stress hyperglycaemia, acute-phase elevation of hs-CRP, and altered lipid metabolism can distort results; defer testing until the patient is in a stable, well state.

variableRecent strenuous exercise

Intense exercise within 24 hours can lower glucose and raise creatinine and uric acid through muscle breakdown and dehydration; advise normal activity but avoid extreme exertion before the test.

elevatesHigh-protein diet and creatine supplementation

Dietary creatine and high meat intake raise serum creatinine and may spuriously lower eGFR; document supplement use and consider cystatin C-based eGFR if the creatinine is unexpectedly high.

reducesB-vitamin supplementation (folate, B12, B6)

Supplementation lowers homocysteine, sometimes masking deficiency or genetic hyperhomocysteinaemia; ideally, test before starting high-dose B vitamins.

variableHaemolysis and sample handling

Haemolysed samples can falsely alter glucose, lipid, and hs-CRP results; refrigerate plasma promptly and avoid prolonged contact with cells.

What do AMP Plus results mean?

Elevated

Elevated fasting glucose and HbA1c indicate prediabetes (5.7–6.4% HbA1c, 5.6–6.9 mmol/L glucose) or diabetes (≥6.5%, ≥7.0 mmol/L), requiring confirmation and risk-factor modification. High fasting insulin and HOMA-IR signal insulin resistance, often preceding glucose abnormalities; combined with elevated triglycerides, low HDL-C, and raised hs-CRP, they define a high-risk metabolic phenotype that warrants intensive lifestyle intervention and consideration of metformin. Elevated LDL-C stratifies cardiovascular risk and guides statin therapy; high hs-CRP adds independent risk information, particularly when LDL-C is borderline. Rising creatinine with falling eGFR points to chronic kidney disease, necessitating blood-pressure control, medication review, and nephrology referral if eGFR <45 or rapidly declining. Elevated uric acid above 420 µmol/L is associated with gout risk and metabolic syndrome; very high levels warrant urate-lowering therapy. Hyperhomocysteinaemia (>15 µmol/L) suggests folate or B12 deficiency, MTHFR polymorphism, or renal impairment, and is treated with B vitamins while investigating the underlying cause.

Normal

Normal glucose, HbA1c, and HOMA-IR indicate preserved insulin sensitivity and low diabetes risk, though HOMA-IR <1.5 is optimal and values approaching 2.0 merit close monitoring. Normal lipids suggest low atherogenic burden, though non-HDL-C and apoB (if available) provide further refinement. Normal eGFR and creatinine indicate preserved kidney function; eGFR 60–89 with no proteinuria or structural disease is often physiological in older adults. hs-CRP <1 mg/L places the patient at low cardiovascular risk; <0.5 mg/L is sometimes described as optimal. Homocysteine 5–10 µmol/L reflects adequate B-vitamin status and low homocysteine-related vascular risk.

Reduced

Low fasting glucose (<3.9 mmol/L) may indicate reactive hypoglycaemia, insulinoma, or adrenal insufficiency and warrants clinical correlation. Low fasting insulin can reflect beta-cell failure in longstanding diabetes or malnutrition. Reduced creatinine is common in individuals with low muscle mass and does not itself indicate disease; interpret eGFR cautiously in such cases. Low HDL-C (<1.0 mmol/L in men, <1.3 in women) is a metabolic-syndrome criterion and signals increased cardiovascular risk, often clustering with high triglycerides. Low uric acid is rarely clinically significant but can occur with proximal tubulopathy or hereditary xanthinuria.

Note: This panel integrates multiple systems and should be interpreted as a whole rather than in isolated pieces. Discordance — normal glucose with high insulin, or low LDL-C with high hs-CRP — is clinically informative and guides targeted follow-up. Serial testing is more powerful than a single result, particularly for tracking insulin resistance and inflammation in response to intervention. eGFR equations have limitations in extremes of body composition and in non-white populations; cystatin C may add precision. HOMA-IR thresholds vary by ethnicity and are less validated than glucose or HbA1c. Homocysteine is a marker, not a treatment target — B-vitamin trials have not demonstrated cardiovascular benefit despite successfully lowering homocysteine. hs-CRP must be repeated if acutely elevated (>10 mg/L) to distinguish chronic low-grade inflammation from intercurrent illness.

Frequently asked questions

The Advanced Metabolic Panel Plus extends the basic metabolic panel by adding fasting insulin, HOMA-IR, full lipid profile, high-sensitivity CRP, and homocysteine, providing detailed assessment of insulin resistance, inflammation, and cardiovascular risk that routine panels miss.

How to access the AMP Plus test

The AMP Plus reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.

Create Free Account

About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:

American Diabetes Association. Standards of Care in Diabetes—2023. Diabetes Care. (2023)
Matthews DR, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. (1985)
Emerging Risk Factors Collaboration. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet. (2010)
Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. (2020)
KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International Supplements. (2013)

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.

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