Fructose and fat cell formation in the body
What it found
High fructose intake is linked to more visceral fat and fat cell formation in people, rats and lab-grown cells.
The authors say fructose in sugary drinks is likely the main culprit.
What they found
Studies in people
Visceral fat in people
In overweight and obese people, drinking a beverage with 25% of daily energy needs as fructose for 10 weeks increased visceral fat compared with a glucose-sweetened drink. A 6-year study found daily sugar-sweetened beverage drinkers had 29% more visceral fat than non-consumers.
Fructose reaches fat tissue
In people, nearly 70% of fructose was metabolized by the liver, and the rest can be used by other tissues including fat tissue. Fat tissue makes the fructose transporter GLUT5, and chronic fructose intake can increase its absorption.
Animal and lab studies
Fat cell formation in lab tests
In lab-grown fat cells and fat precursor cells, fructose alone induced fat cell formation. Fructose increased GLUT5 expression and, in rats, 10% fructose in drinking water increased the number of fat precursor cells and the percentage of differentiated fat cells.
Uric acid and ROS
Fructose metabolism produces uric acid, which in lab tests increased fat cell formation by 50% and raised markers of fat cell growth. Uric acid also increased reactive oxygen species through NADPH oxidase activation in fat cells.
Studies in people and animals
Triglycerides and VLDL
In overweight and obese people, fructose-sweetened drinks for 10 weeks raised blood fats and triglycerides more than glucose drinks. In lab tests, VLDL lipoproteins promoted fat cell formation in 3T3-L1 cells.
Glucocorticoids and fat
Fructose intake increased cortisol in human serum and corticosterone in rat and mouse fat tissue. In rats, 10% fructose in drinking water raised corticosterone in fat tissue and plasma along with fat gain, through higher activity of H6PDH and 11β-HSD1.
What the authors conclude
“In conclusion, high fructose intake has an important role in the current obesity epidemic.”
Also in their conclusions
- They conclude that high fructose intake has an important role in the current obesity epidemic.
- They say the fructose contained in beverages is likely the culprit leading to its excessive intake.
- They state that the capacity of fat tissue to cope with this nutrient overload is exceeded.
How it was done
The authors say there is a lot of evidence that too much fructose harms the liver and other tissues, but less is known about its role in fat cell formation. They wanted to review how fructose affects white fat tissue and the programs that make new fat cells.
They reviewed studies in people, rats, mice and lab-grown cells on how fructose is absorbed and how it affects fat tissue. They looked at human trials giving fructose-sweetened drinks, a 6-year study of sugar-sweetened beverage drinkers, rat and mouse feeding studies, and cell experiments.
What it can’t tell you
- Many of the findings come from rats, mice or lab-grown cells, so they cannot show what happens in people.
- The human studies link fructose intake to more visceral fat, but they cannot prove that fructose alone caused the fat gain.
- The authors say studies with modest fructose intake, especially from fruits, are lacking.
Who paid
- Funding
- Funded by Consejo Nacional de Ciencia y Tecnología (from the PubMed record).
- Conflicts
- The authors declare no conflict of interest.
- Authors work at
- Instituto Nacional de Cardiología Ignacio Chávez, Mexico; Hospital Infantil de México Federico Gómez, Mexico; Instituto Politécnico Nacional, Mexico
The paper
- Title
- High Fructose Intake and Adipogenesis
- Type
- ReviewThe authors read earlier studies and describe what they found. It isn’t a new study.
- Evidence
- Studies in people · animals · lab
- Summarised from
- Full text
- Cite
- Hernández-Díazcouder A, Romero-Nava R, Carbó R, Sánchez-Lozada LG, Sánchez-Muñoz F (2019). High Fructose Intake and Adipogenesis. International journal of molecular sciences. doi:10.3390/ijms20112787Free full textPubMed 31181590DOI
Summary written 26 Sep 2026. Check it against the paper before it changes what you eat. How we summarise papers · Report an error