CME INDIA Presentation by Dr. N. K. Singh, MD, FICP, Director, Diabetes and Heart Research Centre, Dhanbad, Jharkhand, India. Editor,

Does Fructose in Mangoes Raise Sugar?

A video shared on social media, claims that Fructose does not cause blood sugar to rise. Even if you eat plenty of mangoes, blood sugar does not rise. Now diabetics are sharing this with physicians and asking the reality. This post tries to understand the current science on fructose.

“Fructose is structurally different from other sugars like glucose, and it gets metabolized different.”

Untold Story of Fructose: Friend vs Foe

What is Fructose?

  • Fructose is a naturally occurring keto sugar found in its free form in honey, fruit and vegetables and in its combined form as one-half of the disaccharide, sucrose.
  • The main constituents of sugars are fructose and glucose, which can be present either alone or in combination.

Fructose is found in a variety of foods.

  • In table sugar, it is bound to glucose to form the disaccharide sucrose.
  • In honey, it occurs in monosaccharide form.
  • In fruit, berries, and vegetables, fructose occurs in both monosaccharide and disaccharide forms
  • Globally, the main source of fructose is sucrose, which constitutes >90% of the energizing sweeteners used in the world.
  • In some countries, such as USA and Japan, high-fructose corn syrup (HFCS) is also an important source of fructose.
  • HFCS is a mixture of fructose and glucose in different concentrations. It can contain up to 90% fructose.
  • A can of soda –  look at the label – you will  notice a different kind of fructose listed on it, called high fructose corn syrup (HFCS).
  • Be aware, fructose is found in most processed foods from pizza sauce to crackers to breakfast cereal.
  • Fructose is the only sugar that is directly stored in fat cells, which contributes to high triglyceride counts. This is a HUGE problem and is especially true of HFCS in chronic soda-drinkers.
  • 120 Cal Glucose = 1Cal converted to fat. 120 Cal Fructose = 40 Cal converted to fat.

Foods that contain various amounts of natural fructose:

1 medium-sized apple w/skin = 13g of fructose
10 cherries = 4g of fructose
1 medium sized banana = 7g of fructose
1 sweet potato = 0.7g of fructose
5 medium strawberries = 5g of fructose

Fructose does not require insulin to be transported among cells

  • Intake of fructose elicits a low glycaemic index.
  • It does not require insulin to be transported among cells, unlike glucose, that does require insulin.
  • After absorption of fructose, it is transported to the liver where it is effectively absorbed by liver cells.

In the liver, fructose can enter metabolic pathways:
It can be oxidized.
It is converted to glucose (and glycogen).
Or, converted to lactic acid, or enter de novo lipogenesis (DNL).
The other metabolic fate of fructose to form lactic acid only happens at high fructose intakes. Lactic acid can cause muscle soreness and pain.


  • End products of fructose metabolism in hepatocytes are glucose, glycogen, lactate, triglycerides and CO2.
  • Despite the fact that glucose is the main end-product of fructose metabolism in the liver, the glycaemic index following acute ingestion of an oral fructoseload is low compared to glucose and saccharose.
  • After absorption, fructose is transported by the portal vein to the liver, where it is effectively absorbed by liver cells resulting in only small amounts entering the systemic circulation.
  • The concentration of fructose in the blood is therefore only about 0.01 mmol/L, unlike that of glucose which is approximately 5.5 mmol/L.
  • Remember that the liver will metabolize a large majority of the ingested fructose, compared to only about 15–30% of ingested glucose.

Uric acid connection

  • Fructose-induced uric acid generation causes mitochondrial oxidative stress
  • It then stimulates fat accumulation independent of excessive caloric intake.
  • The fructose mediated generation of uric acid may have a causal role in diabetes and obesity provides new insights into pathogenesis and therapies.
  • Fructose intake is a risk factor for hyperuricemia. At present, there seems to be insufficient evidence to support the therapeutic reduction of fructose intake to treat hyperuricemia.

Untold Story of Fructose: Friend vs Foe

Credit: Congwang Zhang, Lijun Li, Yipeng Zhang, Changchun Zeng,Recent advances in fructose intake and risk of hyperuricemia,Biomedicine & Pharmacotherapy,Volume 131,2020,110795,ISSN 0753-3322

When fructose can raise blood glucose?

  • Fructose must be converted to glucose in the liver to cause an increase in blood glucose level.
  • As the conversion takes time and only a portion of the fructose will form glucose, fructose increases blood glucose less than similar levels of glucose
  • The glycaemic index for fructose is only 23
  • So together with lack of stimulation of the pancreatic β cells gives lower insulin secretion after intake of fructose compared with glucose
  • These effects are positive because they contribute to blood glucose homeostasis.

Double edged sword

  • Moderate amounts of fructose have been shown to have positive effects on glycaemic control Fructose may also contribute negatively to blood glucose homeostasis by causing insulin resistance in the liver.
  • There is evidence that a high intake of fructose can cause insulin resistance in animals.

Bottom line

  • Fructose intake must be high to potentially cause insulin resistance.
  • It is conceivable that fructose, via lack of stimulation of satiety signals, could contribute to obesity, but fructose has several properties that act against obesity.
  • The small intestine has a limited capacity to absorb fructose.
  • This can lead to malabsorption at least if large amounts are consumed and consumption occurs without glucose-providing nutrients.
  • Malabsorption of fructose will make less fructose enter the bloodstream and thus less energy will be available to the cells. In this way, the malabsorption will act against obesity.
  • Fructose has a greater thermogenic effect than glucose.

New concept Emerged

  • The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids
  • While it is commonly believed that the liver is the main site of fructose metabolism, Jang et al. show that it is actually the small intestine that clears most dietary fructose, and this is enhanced by feeding.
  • High fructose doses spill over to the liver and to the colonic microbiota.
  • Low doses of fructose are 90% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood.
  • High doses of fructose (1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota).
  • Despite strong ties between fructose and disease, the metabolic fate of fructose in mammals remains incompletely understood.

Do not take high intake of Fructose

  • There are positive effects of fructose, such as high relative sweetness, high thermogenic effect, and low glycaemic index, a high intake of fructose, particularly if combined with glucose, can lead to metabolic changes in the liver.
  • Increased de novo lipogenesis (DNL), and thus altered blood lipid profile, seems to be the most prominent change
  • The distribution of fructose into metabolic pathways, especially DNL, is of key importance to the health effects of fructose.
  • The distribution varies with the amount of fructose consumed.
  • The duration of fructose exposure, the composition of diet/meal matters
  • Individual physiological, enzymatic, and endocrine factors are also important.
  • Dietary fructose intake is increasing.
  • It is increasing primarily from added sugars, including sucrose and high fructose corn syrup.
  • It correlates epidemiologically with the rising prevalence of metabolic syndrome and hypertension worldwide.

Untold Story of Fructose: Friend vs Foe

What is the normal consumption of fructose?

  • Current literature does not indicate that a normal consumption of fructose (approximately 50–60 g/day) increases the risk of atherosclerosis, type 2 diabetes, or obesity more than consumption of other sugars.
  • But a high intake of fructose, particularly if combined with a high-energy intake in the form of glucose/starch, may have negative health effects via DNL.

New Link

  • If your diet is composed of large percentages of fat and fructose, this may lead to development of T2DM.
  • Fructose was first introduced to the western diet to control diabetes based on its low glycaemic index.
  • Hawkins et al in 2022 has shown that fructose-derived glycerate was sustained at high levels in systemic circulation, then chronic glycerate treatment caused damage to pancreatic islet cells, especially β cells.
  • This study suggest that fat consumption enhances intestinal fructose metabolism and circulation of its derived glycerate, which can chronically damage pancreatic islet cells and lead to subsequent glucose intolerance.

Untold Story of Fructose: Friend vs Foe

Credit: Yanru Wu et al, Glycerate from intestinal fructose metabolism induces islet cell damage and glucose intolerance, Cell Metabolism (2022). DOI: 10.1016/j.cmet.2022.05.007


  • Fructose, as in fruits, taken in moderation does not seem to be harmful
  • Diabetics can take 15 to 30 gm of mango and other fruits too in moderation

CME INDIA Tail Piece

  • A high-fat diet is not enough to cause short-term fatty liver disease.
  • If this diet is combined with the intake of beverages sweetened with liquid fructose, the accumulation of fats in the liver accelerates and hypertriglyceridemia can appear.
  • When we eat fruit, the amount of taken fructose is a lot lower compared to a sweetened drink. The process of chewing it and the presence of other elements in the fruit, such as fiber, slows down the absorption of fructose and its arrival to the liver.


  1. The Dark Nasty Truth about Fructose and Type 2 Diabetes (
  2. The Effect of Fructose on Renal Biology and Disease. 2010Journal of the American Society of Nephrology 21(12):2036-9DOI:10.1681/ASN.2010050506
  3. Sugar, Uric Acid, and the Etiology of Diabetes and Obesity .Richard J. Johnson, Takahiko Nakagawa.DIABETES, VOL. 62, OCTOBER 2013
  4. ChREBP‐driven DNL and PNPLA3 Expression Induced by Liquid Fructose are Essential in the Production of Fatty Liver and Hypertriglyceridemia in a High‐Fat Diet‐Fed Rat Model. Molecular Nutrition & Food Research, 2022; 2101115 DOI: 10.1002/mnfr.202101115
  5. Dietary fructose improves intestinal cell survival and nutrient absorption. Nature, 2021; DOI: 10.1038/s41586-021-03827-2

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