Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men

Faeh, David; Minehira, Kaori; Schwarz, Jean-Marc; Periasamy, Raj; Park, Seongsoo; Tappy, Luc

doi:10.2337/diabetes.54.7.1907

Cited by 333 publications

(284 citation statements)

References 39 publications

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“…32 It is likely that most humans are responders to sucrose/fructose overconsumption and that fish oil supplementation inhibits sucrose-induced fatty liver. With respect to HF dietinduced fatty liver, patients with fatty liver have been shown to consume significantly more saturated fat per day than control subjects matched for body mass index.…”

Section: Discussionmentioning

confidence: 99%

Fish oil prevents sucrose-induced fatty liver but exacerbates high-safflower oil-induced fatty liver in ddy mice

Yamazaki

Nakamori²,

Sasaki³

et al. 2007

Hepatology

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Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). We analyzed the effects of dietary fish oil on fatty liver induced by sucrose, safflower oil, and butter in ddY mice. In experiment I, mice were fed a high-starch diet [70 energy% (en%) starch] plus 20% (wt/wt) sucrose in the drinking water or fed a high-safflower oil diet (60 en%) for 11 weeks. As a control, mice were fed a high-starch diet with drinking water. Fish oil (10 en%) was either supplemented or not. Mice supplemented with sucrose or fed safflower oil showed a 1.7-fold or 2.2-fold increased liver triglyceride content, respectively, compared with that of control mice. Fish oil completely prevented sucrose-induced fatty liver, whereas it exacerbated safflower oil-induced fatty liver. Sucrose increased SREBP-1c and target gene messenger RNAs (mRNAs), and fish oil completely inhibited these increases. In experiment II, mice were fed a high-safflower oil or a high-butter diet, with or without fish oil supplementation. Fish oil exacerbated safflower oilinduced fatty liver but did not affect butter-induced fatty liver. Fish oil increased expression of peroxisome proliferator-activated receptor gamma (PPAR␥) and target CD36 mRNA in safflower oil-fed mice. These increases were not observed in sucrose-supplemented or butter-fed mice. Conclusion: The effects of dietary fish oil on fatty liver differ according to the cause of fatty liver; fish oil prevents sucrose-induced fatty liver but exacerbates safflower oil-induced fatty liver. The exacerbation of fatty liver may be due, at least in part, to increased expression of liver PPAR␥.

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Section: Discussionmentioning

confidence: 99%

Fish oil prevents sucrose-induced fatty liver but exacerbates high-safflower oil-induced fatty liver in ddy mice

Yamazaki

Nakamori²,

Sasaki³

et al. 2007

Hepatology

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“…There is ample evidence that increasing the fructose content of the diet increases plasma triglycerides, through several mechanisms, among which are a stimulation of hepatic de novo lipogenesis [26], and a decreased VLDL-triacylglycerol clearance [27]. Based on animal experiments, an increased VLDL-triacylglycerol secretion is also likely to be involved [28].…”

Section: What Are the Mechanisms Responsible For Fructose-induced Metmentioning

confidence: 99%

“…In humans, a high-fructose, hypercaloric diet leads to ectopic fat deposition in liver cells and skeletal muscle in humans already after a 1-wk period [31]. There is strong evidence that fructose decreases hepatic insulin sensitivity in humans [26,32,33], and that a 10-wk high-fructose diet impairs glucose homeostasis in overweight individuals [34]; however, few studies have directly evaluated the effect of a high-fructose diet on whole body insulin sensitivity. It has been reported that supplementation with various amounts of fructose for up to 4 wk failed to decrease whole body insulin sensitivity in healthy individuals [31,35].…”

Section: What Are the Mechanisms Responsible For Fructose-induced Metmentioning

confidence: 99%

Fructose and metabolic diseases: New findings, new questions

et al. 2010

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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...

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confidence: 99%

“…Feeding rats high fructose diet affects both glucose and lipid metabolism which result in a cluster of metabolic abnormalities such as glucose intolerance, hypertension, dyslipidaemia and reduced insulin action (1,2) .…”

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confidence: 99%

Protective role of sardine protein (Sardina pilchardus) against high fructose-induced metabolic syndrome rat

et al. 2010

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Feeding rats high fructose diet affects both glucose and lipid metabolism which result in a cluster of metabolic abnormalities such as glucose intolerance, hypertension, dyslipidaemia and reduced insulin action (1,2) .The aim of the present study was to evaluate the potential influence of sardine protein on biomarkers of oxidative stress and inflammation in high fructose diet-induced metabolic syndrome rat.Male Wistar rats (n = 26) weighing 200°0 g were divided to four groups of six rats each and fed 20% casein (Cas) or sardine protein (SP) with or without 64 % fructose (F) for 2 months. Plasma glucose, insulin, lipids, tumour necrosis factor-a and leptin levels were determined. Lipid peroxidation and hydroperoxydes, vitamin (Vit) E and Vit C and antioxidant enzymes activities in liver homogenates were assayed.The SPF diet diminished by 21 % and 51 % plasma glucose and glucose intolerance as compared to CasF (P < 0.05). Plasma glucose was increased by 39 % and 28 % in CasF and SPF as compared to Cas and SP, respectively. Plasma insulin levels were reduced by 35 % in SPF v. CasF and by 38 % in SP v. Cas but were increased by 31 % in SPF v. SP. HOMA-IR index was 1.72-and 1.91-fold lower in SPF v. CasF and in SP v. Cas, respectively. Moreover, HOMA index was enhanced by 47 % in CasF v. Cas and 64 % in SPF v. SP. Plasma cholesterol, triglycerides and free fatty acids levels were significantly lower in SPF and SP rats compared to CasF and Cas. Consumption of SP diet with or without fructose lowered significantly plasma TNF-a values as compared with casein. The high fructose in both the protein diets increased plasma TNF-a by 98 % in CasF v. Cas and by 143% in SPF v. SP. Plasma leptin was lower 1.23-fold in SPF than CasF and 2.40-fold in CasF than Cas and 2.28-fold in SPF than SP. Liver hydroperoxides concentrations were enhanced by 18 % and 11 % in CasF v. Cas groups and in SPF v. SP groups, respectively. Lowered values were noted in liver superoxide dismutase activity in CasF v. Cas (38%) and in SPF v. SP (34%). Glutathione peroxidase activity was 1.6-and 1.42-fold lower in CasF v. Cas and in SPF v. SP, respectively. No significant difference was observed in catalase activity. Feeding SP diet with or without fructose increased significantly liver Vit C. Hepatic Vit C contents were reduced by 39 % in CasF v. Cas and 33 % in SPF v. SP. Liver Vit E was significantly higher in SP v. Cas. In addition, Vit E levels were 1.53-and 1.63-fold lower in CasF v. Cas and in SPF v. SP rats.In conclusion, sardine proteins have hypoglycaemic, hypoinsulinaemic and hypolipidaemic effects and improve oxidative and inflammatory stress induced by a high-fructose diet, suggesting that these proteins may have a beneficial action on functional characteristics of pancreatic beta cells, probably by improving insulin and thereby insulin resistance prevention and may contribute to the low risk of coronary heart disease in patients with the metabolic syndrome.

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Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men

Cited by 333 publications

References 39 publications

Fish oil prevents sucrose-induced fatty liver but exacerbates high-safflower oil-induced fatty liver in ddy mice

Fish oil prevents sucrose-induced fatty liver but exacerbates high-safflower oil-induced fatty liver in ddy mice

Fructose and metabolic diseases: New findings, new questions

Protective role of sardine protein (Sardina pilchardus) against high fructose-induced metabolic syndrome rat

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