Dietary Fructose and Glucose Differentially Affect Lipid and Glucose Homeostasis
sugars, fructose, high-fructose corn sugar, sucrose, metabolism Historically, much of the emphasis on the relation between nutrition and CVD National Goals for Cardiovascular Health Promotion and Disease Reduction” (11). glucose, this represents a mean of roughly kcal/(person ⋅ d) of each of. Absorbed glucose and fructose differ in that glucose largely escapes . data would suggest little difference in the effects of sucrose compared with HFCS, In humans in the fed state, ∼2 mg/(kg·d) of apoB is secreted into plasma and its No clear goals for TG or HDL-C levels have been established by the NCEP (1). Journal of Nutrition. The goals for this learning module are listed on the slide. . In take. (g. /cap ita/d.) HFCS, Free and Total Fructose Consumption . •Data are not compelling for a significant difference in satiating effects of.
This led some scientists to question the importance of fructose as a means for stimulating lipid synthesis and accumulation. However, the importance of fructose reemerged with a report in this journal linking intake of sugary sweetened beverages, and in particular fructose, with non-alcoholic fatty liver disease NAFLD 11an association that has been confirmed in numerous other studies and is now a major area of research 12 — Here we provide an update on the association and potential mechanisms by which fructose causes fatty liver.
One of the key findings is that it is not the fructose molecule itself that is primarily responsible for making triglycerides, but rather fat accumulates in the liver by the general activation of lipogenesis while at the same time blocking fatty acid oxidation 16 The Discovery of NAFLD and Its Association with Metabolic Syndrome An association of diabetes with liver disease and gout has been known for over years 18 and is strongly associated with insulin resistance.
Type 2 diabetes mellitus is the strongest predictor for NAFLD-related hepatic fibrosis and cirrhosis However, the recognition that people with obesity and prediabetes could develop NAFLD emerged only in the last several decades 20 — Many patients with NAFLD show characteristics observed in subjects with metabolic syndrome, including elevated plasma triglycerides, low HDL cholesterol, impaired fasting glucose levels, an increased waist circumference, and elevated blood pressure Indeed, NAFLD can be viewed as another clinical manifestation of metabolic syndrome, similar to that of hyperuricemia, systemic inflammation elevated C reactive proteinand microalbuminuria.
NAFLD was not recognized as a clinical entity until the s 20 — 22but has been increasing in prevalence, and may progress to nonalcoholic steatohepatitis NASH or cirrhosis and eventual liver transplantation 24 NAFLD is also the most common chronic liver disease in children and adolescents especially in obese patients and has even been detected in infants of mothers with gestational diabetes, making this disorder relevant across a wide spectrum of ages 26 — Soft Drinks and Added Sugar are Associated with Fatty Liver While fructose is present in honey and fruits, the major source of fructose is from sucrose and HFCS, especially in sugary sweetened beverages.
Experimental Studies Dietary fructose, sucrose, or HFCS have been shown to have a special tendency to induce fatty liver in experimental animals 61730 — 34as well as inflammation To develop the fatty liver, it usually takes atleast 8—24 weeks on high fructose diet with more progressive disease with longer exposure Often the administration of fructose also induces other features of metabolic syndrome as well, including elevated blood pressure, elevated serum triglycerides, and insulin resistance To the concept of GI has been added the concept of glycemic load, which is the product of GI of the food and its carbohydrate content.
There is a major body of literature indicating that diets with a high GI and glycemic load are more likely to promote increased TG levels, decreased HDL-C levels, and increased indices of insulin resistance over time compared with low-GI diets.
Therefore, classification of foods on this basis may be helpful in the prevention and treatment of type 2 diabetes.
However, there is much debate about this topic and it can be argued that a focus on specific types of dietary carbohydrates may also have scientific merit and provide more specificity 5. Plasma lipoprotein metabolism A variety of lipoproteins exist in human plasma that differ in their density, lipid composition, and electrophoretic mobility 2.
After the ingestion of a fat-rich meal, hydrolysis of TG to fatty acids and their absorption, these fatty acids are again placed onto a glycerol backbone in the intestine and packaged into large TG-rich chylomicrons. An enzyme-linked immunoassay for apoB is now available, which is specific for this protein the only available marker for intestinal TG-rich particles or chylomicrons 16 — CHD patients also often have elevated postprandial TG levels compared with controls Excess fructose and fat uptake by the liver has a deleterious effect on liver metabolism, causing increased liver fat, increased VLDL-TG, and apoB secretion as well as increased secretion of the inflammatory markers C reactive protein, fibrinogen, and serum amyloid A by the liver into the plasma space.
Remnant lipoprotein cholesterol assays are available, which measure remnant lipoproteins of both liver and intestinal origin 21 — Moreover, elevated remnant lipoprotein cholesterol levels are elevated in CHD patients compared with controls in both the fasting and fed state, especially in women and in individuals with diabetes 91021 — LDL is the most atherogenic of lipoprotein particles, is enriched in cholesteryl ester, and has been divided into large LDL 1.
LDL particle subspecies can be measured by vertical rotor ultracentrifugation, NMR, or gradient gel electrophoresis 8 However, all these assays are labor intensive and have not been well standardized.
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These assays also avoid the problems of calculating LDL-C 25 — The levels of these lipoproteins can be lowered with diet and by statin treatment 28 — Another atherogenic lipoprotein is Lp awhich is an apoB particle, usually an LDL particle, with a protein known as apo a attached to the terminal region of apoB by a disulfide bond. Apo a has significant homology with plasminogen and may interfere with the ability of plasminogen to promote clot lysis.
An elevated Lp a has been shown to be an independent CHD risk factor and Lp a can be lowered with niacin therapy. Lp a values in plasma or serum are generally measured by immunoassay, although assays for Lp a cholesterol have also been established 12 The major function of HDL is to serve as an acceptor of cholesterol from tissues and to deliver it to the liver for excretion from the body in the bile 13 — 1534 Diets high in saturated fat and cholesterol raise LDL apoB by delaying its fractional clearance and increase HDL apoA-I production in humans probably a compensatory effect 2.
Very little information is available on specific types of dietary carbohydrate on lipoprotein metabolism. Our own data indicate that 4 wk is the minimum time needed to arrive at a new steady state for plasma lipoprotein concentrations under controlled isocaloric conditions when the composition of the diet has been altered 2. Here we review the most important and relevant human studies. Reiser 39 reviewed the literature and concluded that individuals with elevated insulin and TG levels were more likely to have deleterious effects on glucose and lipid metabolism from diets high in sucrose and fructose than normal individuals.
Steiner 40 came to similar conclusions and indicated that diets high in simple carbohydrates increased VLDL-TG production. In both groups, these investigators noted significantly higher levels of TG, total cholesterol, and uric acid with the high-fructose diet, with significant increases in VLDL-C in the hyperinsulinemic men and significant increases in LDL-C in normoinsulinemic men.
They concluded that dietary fructose had a deleterious effect on cardiovascular risk, especially in the men with hyperinsulinemia. They noted that the fructose diet resulted in significant increases in total cholesterol and LDL-C compared with the high-starch diet and fasting and postprandial TG, insulin, and glucose levels did not differ.
These investigators 49 conducted identical studies in 6 patients with type 1 diabetes and 12 patients with type 2 diabetes. Similar effects were seen in both types of diabetics. Mayes 51 reviewed the topic and concluded that fructose had deleterious effects on lipids because of its rapid uptake and utilization by the liver, resulting in increased VLDL-TG secretion.
Long-term effects include decreased glucose tolerance and insulin resistance and increased uric acid production in animals. Gerrits and Tsalikian 53 reviewed the topic and concluded that short-term studies indicate that replacing sucrose with fructose improved glycemic control in diabetic subjects, but that long-term studies were needed.
Levels of other lipoproteins were apparently measured but not reported. Both types of meals raised TG levels, but the fructose meal raised VLDL Sf 20— particles TG, but not chylomicron TG, substantially more than the high-glucose meal, with the greatest differences observed at 6 h after the meal. De novo lipogenesis did not differ between the 2 meals.
The authors concluded from their studies that the greater increase in VLDL-TG was not due to excess production but rather to delayed clearance.
Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease
They speculated that these effects may have been due to less insulin stimulation and less insulin-stimulated increases in lipoprotein lipase activity, but they did not measure this latter parameter McAuley 63 reviewed the topic of nutritional factors and insulin resistance and concluded that excess amounts of dietary energy, saturated fat, fructose, and glucose and lack of fiber have all contributed to the potential for developing insulin resistance.
Conclusions Investigators began recommending the use of fructose instead of glucose, because acutely, it did not raise blood glucose or insulin levels, in contrast to glucose. However, the price for this potential benefit is rapid uptake by the liver and often conversion into TG. Diets high in fructose are a common way to induce features of metabolic syndrome in rodent models Moreover, quite a substantial body of literature indicates that dietary fructose plays a role in causing nonalcoholic liver steatosis 64 The same statement can be made for HFCS.
Stanhope and Havel 66 have reported in an ongoing study that a high-fructose diet, but not a high-glucose diet, increases visceral adiposity, promotes dyslipidemia, and increases insulin resistance. They postulated that dietary fructose preferentially causes postprandial hypertriglyceridemia, promotes visceral adiposity, hepatic lipid accumulation, protein C kinase activation, and hepatic insulin resistance.
Stanhope and Havel 67 have recently reported no significant differences between sucrose and HFCS with regard to short-term effects on fasting and postprandial TG, glucose, insulin, leptin, and ghrelin levels. The level of dietary fructose used in many of the quoted studies is much higher than that found in typical diets.
Significant changes were not observed when fructose vs. In addition, the increase in dietary fructose has not been disproportionate to the increase in energy, fat, and cereal grains between the s and the present. Available data suggest that a sedentary lifestyle, an abundance of energy and fast food, smoking cessation, and diets containing excess energy, saturated fat, sucrose, and HFCS have all contributed to our current epidemic of obesity and type 2 diabetes.
The food industry can help ameliorate this situation by providing the consumer with better food options that are lower in simple carbohydrate, saturated fat, trans fat, and cholesterol and are richer in essential fatty acids, fiber, and complex carbohydrate. Other articles in this supplement include 69 — Notes 1Published in a supplement to The Journal of Nutrition.
What is the relationship between D-glucose and D-fructose?
The views expressed in these papers are not necessarily those of the USDA, the Agricultural Research Service, or the supplement coordinators. Supplement coordinators for this supplement were David M. Kretsch, no conflicts of interest. In the s the caries theory was depicted as 3 circles representing the 3 prerequisites for dental caries: Since then, many modifying factors have been recognized, resulting in a more complex model that includes saliva, the immune system, time, socioeconomic status, level of education, lifestyle behaviors, and the use of fluorides.
An important breakthrough in the understanding of dental caries was the recognition of the remineralization process as a result of plaque fluid and saliva at pH levels above a critical value being highly saturated with calcium and phosphates. The caries process can be described as loss of mineral demineralization when the pH of plaque drops below the critical pH value of 5. Redisposition of mineral remineralization occurs when the pH of plaque rises.
The presence of fluoride reduces the critical pH by 0. Whether a lesion develops is the outcome of the balance between demineralization and remineralization, in which the latter process is significantly slower than the former.