What markers track de novo lipogenesis?
De novo lipogenesis is tracked in research by enzyme markers such as FASN and by lipid species that accumulate when the pathway is active. This page summarises what the cited studies measured and in which models.
De novo lipogenesis (DNL) is the metabolic pathway that builds fatty acids from non-lipid precursors, principally acetyl-CoA, and it is tracked in research by two broad classes of markers: the enzymes that catalyse the pathway, of which fatty acid synthase (FASN) is described in the cited literature as the rate-limiting enzyme, and the lipid species that accumulate downstream when the pathway is active, including ceramides and the hepatic lipid pool measured in steatosis [2][1]. The formal pathway name is de novo lipogenesis; it is a cytosolic biosynthetic route rather than a receptor family, and the work cited here centres on the FASN-catalysed step and on hepatic lipid accumulation in insulin-resistant states [2][1].
Identifiers vary by marker and by study, and the evidence block for this page does not supply a sequence, formula or molecular weight for any single marker, so none is stated here.
Research Studies
FASN and ceramide accumulation in arrhythmogenic cardiomyopathy
In arrhythmogenic cardiomyopathy (ACM), a heritable disease caused by desmosomal gene mutations and characterised by progressive myocardial loss and fibrofatty replacement, FASN was reported to be upregulated in cardiomyocytes of ACM patients and of a corresponding model [2]. The same work reported that FASN-mediated de novo lipogenesis promotes ceramide accumulation and myocardial damage in that disease context [2]. This is a disease-specific finding in a heritable cardiomyopathy population, not a general statement about DNL in healthy tissue.
Hepatic lipid accumulation and the NAFLD diagnostic threshold
Non-alcoholic fatty liver disease (NAFLD) is defined as excessive lipid accumulation within hepatocytes in the absence of significant alcohol consumption or other causes of chronic liver disease [1]. The cited clinical study reports that NAFLD affects 25% to 30% of the global population and nearly one third of the population in North America, and that the minimum criterion for a histologic diagnosis is greater than 5 percent lipid content [1]. These figures describe the hepatic lipid endpoint that DNL markers are used to interrogate, not a marker measurement itself.
Insulin resistance and the clinical features accompanying hepatic steatosis
The same clinical study describes the presentation of these patients: hepatic steatosis observed on imaging studies, elevated liver enzymes, and clinical features of insulin resistance, including pre-diabetes, type 2 diabetes mellitus, arterial hypertension, dyslipidemia and visceral obesity [1]. This population framing matters for marker interpretation, because the metabolic context in which a DNL marker is measured is part of what the measurement means.
Diet and hepatic transcriptomics in pre-diabetes
The clinical study cited here is titled around diet impact on hepatic transcriptomics and lipidomics in pre-diabetes, indicating that both transcript-level and lipid-level readouts were collected in that population [1]. The evidence block does not report the specific transcripts, lipid species or effect sizes from that study, so no values are given here.
Comparing the two marker classes
| Marker class | Example in the cited evidence | Model or population | What it reflects |
|---|---|---|---|
| Pathway enzyme | FASN, described as the rate-limiting enzyme of DNL [2] | Cardiomyocytes of ACM patients and a corresponding model [2] | Upregulation of the lipogenic enzyme programme |
| Downstream lipid species | Ceramides [2] | ACM myocardium [2] | Accumulation of products downstream of DNL |
| Hepatic lipid pool | Steatosis above the histologic threshold [1] | NAFLD and pre-diabetic populations [1] | Net hepatic lipid content, not flux through DNL alone |
Where the evidence is disease-specific rather than general
The FASN and ceramide findings come from a heritable cardiomyopathy context [2]. The hepatic lipid and insulin-resistance findings come from a clinical study in pre-diabetic and NAFLD populations [1]. Neither source in the evidence block supports a claim about DNL marker behaviour in healthy humans at rest, and no such claim is made here.
What the evidence does not establish
- No quantitative reference range for any DNL marker is given in the evidence block.
- No comparison of marker performance between assays is given.
- No human dose, exposure or intervention data are given.
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