The obesogenic effects of polyunsaturated fatty acids are dependent ...

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Although fructose has long been used to induce glucose intolerance in rats, in C57BL/6 mice neither hyperinsulimia nor hyperglycemia is developed. It had been shown C57BL/6 mice are lessresponsive towards fructose-induced Srebf1 activation among different strains of mice due to a single nucleotide polymorphism in the promoter region 72 . However we failed to observe this unresponsiveness. As others have shown in rats 73 , in our fructose-fed mice despite the presence of fish oil in the diet, lipogenic genes were induced and β-oxidation-related targets were repressed (Fig.2.2F). But when compared to sucrose- and glucose-fed mice, these animals gained least body weight, had the lowest amounts of fat tissues and lowest circulating triglycerides (Fig2.2), so the extra fat has to be either stored ectopically or burnt. The increased brown adipocyte phenotype in the iWAT could, in part, assist this process. Although others have shown the development of hepatic lipid accumulation in fructose-fed mice 74 , it was not the case in our hands despite elevated liver to body weight ratios (Fig2.3A). Interestingly, the authors also reported that a nonabsorbable antibiotics treatment could attenuate lipid accumulation in liver, suggesting potential involvement of gut microbes in fructose metabolism 74 . The metabolic effects of fructose do not limit to the listed above, as there have been reports showing centrally-administrated fructose led to increased food intake in rodents 75,76 by reducing hypothalamic malonyl–CoA levels 76 . Furthermore, the ability of fructose to cross the blood-brain barrier indirectly supports this observation, as the orexigenic effect relies on CNS function 77 . One interesting study, by using hyperinsulinemic-euglycemic clamps, demonstrated that sucrose feeding was not the same as with the combination of its hydrolysis products glucose and fructose in promoting hepatic insulin resistance 78 . This may suggest the involvement of gastric emptying or the release of gut-secreted hormones. Fish oil contaminants Long chain n-3 fatty acids in fish oil are not synthesized de novo by fish themselves, but by algae they consume in the wild or added to the feed in farmed fish colonies 79 . Along with the beneficial nutrients, through food chains, persistent organic pollutants (POPs) are also accumulated. Despite the effort to limit their release, POPs still persist in the environment 80 . POPs such as organochlorine pesticides, polychlorinated biphenyls (PCBs) and dioxins are hydrophobic compounds, and consequently they accumulate in fatty tissues, and therefore are inevitably retained in the process of fish oil production. 14
In a pair of population studies, an association was reported between serum concentrations of POPs and insulin resistance in spite of the subjects’ diabetic status 81,82 . Furthermore, different mechanisms were proposed in explaining this deteriorating effect, which include causing mitochondrial dysfunction 83 and impairment of insulin actions both in vivo and in vitro (ref 84 , Annex 5). In order not to weigh out the beneficial effect by pollutants, purity would be a major concern when consuming very long chain marine n-3 fatty acids. This also applies to the use of fish oil in animal feeds 85 . 15
Page 1 and 2: The obesogenic effects of polyunsat
Page 3 and 4: Table of Contents Acknowledgement .
Page 5 and 6: Abstract in Danish Polyumættede n-
Page 7 and 8: Polyunsaturated fatty acids in the
Page 9 and 10: was more than 3 times higher in the
Page 11 and 12: gluconeogenesis and ureagenesis (Fi
Page 13: high dietary PUFAs, the modulation
Page 17 and 18: 18. Massiera, F. et al. Arachidonic
Page 19 and 20: 54. Xu, J. et al. Polyunsaturated f
Page 21 and 22: Annexes 1. Ma T, Liaset B, Hao Q, P
Page 23 and 24: Fish Oil, Sucrose and Obesity Obesi
Page 25 and 26: Fish Oil, Sucrose and Obesity Figur
Page 27 and 28: Fish Oil, Sucrose and Obesity Table
Page 33 and 34: Fish Oil, Sucrose and Obesity 6. Ma
Page 35 and 36: Carbohydrate source and insulin sec
Page 37 and 38: 20 21 22 23 24 25 26 27 28 29 30 31
Page 39 and 40: 68 69 70 71 72 73 74 75 76 77 78 79
Page 41 and 42: 114 115 116 117 118 119 120 121 122
Page 43 and 44: 160 161 162 163 164 165 166 167 168
Page 45 and 46: 208 209 210 211 212 213 214 215 216
Page 47 and 48: 256 257 258 259 260 261 262 263 264
Page 49 and 50: 302 303 304 305 306 307 308 309 310
Page 51 and 52: 350 351 FIGURE LEGENDS 352 353 354
Page 53 and 54: 398 399 400 401 402 403 404 subunit
Page 55 and 56: 446 447 448 449 450 451 gamma, coac
Page 57 and 58: 484 485 486 TABLE 1. Macronutrient
Page 59 and 60: Energy (kJ/g) 17.16 25.12 25.12 25.
Page 61 and 62: 561 562 563 564 565 566 567 568 569
Page 63 and 64: 635 636 637 638 639 640 641 642 643
Page 65:
711 712 713 714 715 716 717 718 719
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Cyclooxygenases and UCP1 Although i
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Cyclooxygenases and UCP1 Figure 2.
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Cyclooxygenases and UCP1 Figure 4.
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Cyclooxygenases and UCP1 PLoS ONE |
Page 82 and 83:
Cyclooxygenases and UCP1 E synthase
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Cyclooxygenases and UCP1 29. Granne
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JBC Papers in Press. Published on J
Page 88 and 89:
hydrolysate (SPH), would be protect
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was used as the liver cytosolic fra
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In order to demonstrate that bile a
Page 94 and 95:
Nutritional regulation of endogenou
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in increased whole body energy expe
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38. Kanehisa M, and Goto S. (2000)
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FOOTNOTES This work was carried out
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fed the same diets, plus the SPH-di
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Figure 2 A nmol/ min/ mg prot 2,4 1
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Figure 4 A 6 Liver Pparα B 21 Live
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Figure 7 A Plasma ALAT B Liver Ucp2
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Ruzzin et al. investigated the meta
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Ruzzin et al. CD14, and rho kinases
Page 114 and 115:
Ruzzin et al. salmon oil induced a
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The obesogenic effects of polyunsaturated fatty acids are dependent ...

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