Fructose and metabolic diseases: New findings, new questions

Abstract

There has been much concern regarding the role of dietary fructose in the development of metabolic diseases. This concern arises from the continuous increase in fructose (and total added caloric sweeteners consumption) in recent decades, and from the increased use of high-fructose corn syrup (HFCS) as a sweetener. A large body of evidence shows that a high-fructose diet leads to the development of obesity, diabetes, and dyslipidemia in rodents. In humans, fructose has long been known to increase plasma triglyceride concentrations. In addition, when ingested in large amounts as part of a hypercaloric diet, it can cause hepatic insulin resistance, increased total and visceral fat mass, and accumulation of ectopic fat in the liver and skeletal muscle. These early effects may be instrumental in causing, in the long run, the development of the metabolic syndrome. There is however only limited evidence that fructose per se, when consumed in moderate amounts, has deleterious effects. Several effects of a high-fructose diet in humans can be observed with high-fat or high-glucose diets as well, suggesting that an excess caloric intake may be the main factor involved in the development of the metabolic syndrome. The major source of fructose in our diet is with sweetened beverages (and with other products in which caloric sweeteners have been added). The progressive replacement of sucrose by HFCS is however unlikely to be directly involved in the epidemy of metabolic disease, because HFCS appears to have basically the same metabolic effects as sucrose. Consumption of sweetened beverages is however clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through an increase in body weight. This has led to the recommendation to limit the daily intake of sugar calories.Pure, white, and deadly: the dark side of sugar was suspected many years ago, when an association between sugar consumption and coronary heart diseases was recognized and emphasized by John Yudkin [1]. Sugar, a natural sweetener obtained from either sugar cane or beets, is a disaccharide composed of one glucose molecule linked through an α1-4 glycoside bond to a fructose molecule. Fructose, besides contributing to half the total content of sugar, can also be found as a hexose in fruits and honey. More recently, sweeteners started to be produced from corn through starch isolation and hydrolysis to glucose, followed by enzymatic isomerization of part of the glucose into fructose [2,3]. The resulting mixture, known as high-fructose corn syrup (HFCS), has several industrial advantages over sugar, the most important being its low price, and has progressively replaced sugar consumption in North America over the past 30 years.Fructose metabolism has been reviewed extensively elsewhere [4][5][6] and will be only briefly outlined here. In the gut, fructose is transported by specific transporters, GLUT5 [7,8]. In some subjects, fructose absorption is quantitatively limited, and some malabsorption occurs when lar...

Sugar-sweetened beverages, vascular risk factors and events: a systematic literature review

“…Studies show that added sugar (over-) consumption, specifically in the form of sugar-sweetened beverages (SSB), seems to be linked to different harmful health outcomes such as obesity and diabetes (3)(4)(5) . SSB may also potentially increase the risk of CVD through their high amount of rapidly absorbable carbohydrates that may, via an elevated hepatic de novo lipogenesis, result in hypertension, accumulation of visceral and ectopic fat, and increased TAG and LDL cholesterol (LDL-C) and decreased HDL cholesterol (HDL-C) levels (6,7) . The increased glycaemic load caused by a high SSB intake may lead to inflammation, β-cell dysfunction and insulin resistance, as suggested by who, in their pooled meta-analysis from three prospective cohorts, reported that participants in the highest category of SSB intake had a 20 % greater risk of developing metabolic syndrome than those in the lowest category of intake (4) .…”

Fruit and vegetable consumption and all-cause, cancer and CVD mortality: analysis of Health Survey for England data

“…9 This may reflect different types of fruit and/or vegetables consumed by different Table 4 Association between portions of fruit or of vegetables consumed and risk of death, from all causes unless specified populations, and merits further consideration, particularly given current interest in the role of fructose in driving obesity. [29][30][31] When individual types of fruit and vegetables were examined, portions of fresh vegetable, salad, fresh and dried fruit showed significant negative associations with all-cause mortality. It has been suggested that some fructose consumption in levels provided by fruit may be beneficial for glycaemic control.…”

End hunger, achieve food security and improved nutrition and promote sustainable agriculture

“…Doubling agricultural productivity (2.3) could constrain the reduction of premature mortality from non-communicable diseases (3.4) if this increase focuses on lownutrient and energy-rich foods, such as cereals, tubers, and fats. These agricultural products are contributing to the triple burden of undernutrition, micronutrient deficiency, and obesity with its associated health issues, such as stunting, anaemia, and diabetes (Tappy et al, 2010). The poor are adversely affected in this respect because energy-rich, low-nutrient foods are becoming more affordable to them worldwide (Bernard, 2015).…”