Liver fat accumulation ranks among the most frequently flagged conditions on routine health screening reports across India, yet it tends to go unaddressed by a large share of those who receive the diagnosis. Among the 2,373 adults between 18 and 30 examined in Thiruvananthapuram district — a group drawn largely from non-obese, non-drinking participants — roughly one in four carried the condition.
Published in 2024, the research identifies two distinct health trajectories tied to liver fat: its accumulation raises the likelihood of developing heart disease or diabetes, while any subsequent scarring places the organ itself at elevated risk. Insulin resistance underlies a liver condition — now officially designated metabolic dysfunction-associated steatotic liver disease, or MASLD, following a 2023 nomenclature update — that develops in people whose body weight falls within a normal range.
Under normal conditions, fat tissue responds to insulin by retaining its energy reserves; once that hormonal signal goes unheeded, adipose cells discharge fatty acids into the bloodstream at an unchecked rate, leaving the liver to absorb the overflow and deposit whatever it cannot convert into fuel. A 2006 PNAS study conducted at Yale found that South Asian men of slender build showed insulin resistance at rates three to four times higher than those recorded among white male participants of comparable age, with hepatic fat levels running roughly double in the South Asian group.
According to Dr. Shiv K. Sarin, who heads the Institute of Liver and Biliary Sciences (ILBS) in Delhi, roughly one in ten people diagnosed with fatty liver fall into the young, normal-weight category — a group that, in his assessment, tends to present with elevated blood fats and blood sugar readings in the prediabetic range. As the condition advances, lipids arrive at the liver more rapidly than hepatocytes can process or accommodate them, harmful metabolic waste accumulates, cellular death follows, and the immune system mounts an inflammatory response.
When cells die, the distress signal they release rouses stellate cells — ordinarily quiescent and holding reserves of vitamin A — into producing collagen, the fibrous protein that forms scar tissue. Liver scarring follows a five-point scale running from F0 through F4, with the F4 designation marking the condition known as cirrhosis.
Fatty liver alone rarely advances to a worse stage, and for the majority of those affected, Sarin notes, cardiovascular health poses the more pressing concern. Among 17,301 patients who underwent liver biopsy, published findings in Clinical Gastroenterology and Hepatology (2023) placed the likelihood of liver-disease death at 7.6 times greater for those at fibrosis stage F3 compared with those showing no fibrosis, and at 15 times greater for those at stage F4; Sarin noted that both liver fat and liver fibrosis require evaluation.
When the source of damage is removed, stellate cells either revert to an inactive state or die, allowing the liver's own enzymes to progressively dismantle the accumulated collagen — a process through which fibrosis can reverse. Evidence from trials of a pair of medications points to measurable benefit for patients.
In a 52-week trial published in the New England Journal of Medicine in 2024, roughly one in four patients taking resmetirom — an oral drug that targets the THR-beta thyroid hormone receptor in the liver, prompting hepatic cells to metabolise fat at a higher rate — showed fibrosis regression of at least one stage, compared with 14.2 percent among those receiving a placebo. At the 72-week mark in a 2025 New England Journal of Medicine study, liver-scarring reversal was recorded in roughly 37% of participants receiving semaglutide — a GLP-1 hormone analogue whose hepatic effects are thought to flow largely through body-weight reduction — compared with about 22% among those who did not receive it.
Regulatory clearance in the United States rests on biopsy findings alone for both drugs, long-term outcomes data on cirrhosis prevention or mortality have yet to materialise, and the trial populations skewed toward considerably higher body weights — averaging around a BMI of 35 — than those typical among Indian patients. Administered over 96 weeks to 181 participants in a phase 2 trial, efruxifermin — a compound that mimics FGF21, a hormone involved in regulating fat metabolism and suppressing the biological pathways associated with tissue scarring — produced histological improvement in 29% of those receiving it, versus 11% among those on placebo, a result that positions it as the first therapy backed by randomised data showing partial reversal of cirrhosis.
Regulatory clearance for saroglitazar — a domestically developed compound — came in 2020, resting on a single trial funded by its manufacturer that enrolled 102 participants and tracked disease activity without assessing fibrosis progression. The drug has yet to receive regulatory clearance for use within India.
Among available interventions, weight-loss approaches tend to be backed by a comparatively larger body of research than most alternatives. Of those who shed a tenth of their body weight over twelve months, liver inflammation cleared up in nine out of ten cases, while tissue scarring showed measurable reversal in nearly half. Sarin notes that none of the medications can take the place of maintaining a low-carbohydrate, low-fat diet alongside routine physical activity.
Locating the scar presents a challenge of its own. Because FIB-4 is calculated partly from a patient's age, the score tends to register lower in younger people — and the European guideline itself acknowledges that the tool does not perform reliably in those under 35. Sarin has called for basket trials designed to assess a drug's effect across the full metabolic spectrum — covering liver fat reduction, lipid levels, diabetes, cardiovascular disease risk, and longevity outcomes.
Long-term tracking of non-obese young adults in India who develop fatty liver disease has not been carried out at a scale or duration that would clarify whether cirrhosis progression in that population moves at a different pace from the trajectory documented among heavier patients in Western clinical datasets.
