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

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279 280 281 282 283 284 285 286 287 288 289 290 by administration of nifedipine attenuated the adipogenic effect of fish oil in combination with sucrose. Increasing insulin secretion alone, however, is not sufficient to promote obesity development, as mice receiving glybenclamide in combination with proteins and fish oil did not become obese. Furthermore, increased insulin secretion by glybenclamide in the presence of low levels of carbohydrates in the feed was insufficient to increase the adipogenic potential of fish oil. It has been demonstrated that a high-fat diet is unable to increase adipose tissue mass in the absence of carbohydrates (55, 56). In our study nifedipine did not reduce adipose tissue mass in low fat fed mice (not shown). However, as emphasized above, inclusion of nifedipine attenuated hyperinsulinemia and obesity induced by fish oil in combination with sucrose. These findings are in line with the study by Kim et al (34) demonstrating that nifedipine attenuated agouti-induced hyperinsulinemia and 291 obesity. Hyperinsulinemia is an early event also in obese Zucker rats, and attenuation of 292 293 294 295 296 297 298 299 300 301 hyperinsulinemia using diazoxide reduces obesity development in obese- but not lean Zucker rats independently of feed intake (57). Together our results suggest that the increased insulin secretion contribute to the obesity promoting effect of fish oil when combined with sucrose. The obesity promoting effect of increased insulin secretion is further supported by our finding that glucose, but not fructose is the obesity promoting moiety of sucrose. Unlike sucrose and glucose, fructose does not stimulate insulin secretion from pancreatic beta-cells (26) and mice receiving fish oil in combination with fructose had less adipose tissue mass than mice receiving fish oil in combination with glucose or sucrose. Mice receiving fructose in combination with fish oil were also less glucose intolerant than mice fed fish oil in combination with sucrose or glucose. Fructose is commonly used to induce glucose intolerance in rats and some mice strains also develop 14
302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317 318 319 320 321 322 323 324 325 metabolic syndrome in response to high fructose feeding (58). However, in C57BL/6 mice neither hyperinsulinemia nor hyperglycemia developed in response to high fructose feeding (58). The obesity promoting effect of fish oil can also be affected by different type of starch as mice receiving fish oil in combination with a high GI starch had higher adipose tissue mass than mice receiving fish oil in combination with low GI starch. These results may also relate to the effect of the different type of starch on postprandial glucose levels and insulin secretion (33, 42, 59). Low GI diets are becoming popular in weight management also in humans although their effectiveness in terms of lasting weight reduction is not commonly accepted (28-32). The lack of acceptance may, however, partly be due to insufficient power of early studies as a meta-analysis has indicated that diets in which there was a reduction in the glycemic index produced moderately more weight loss than control low fat diets in humans (32). However, a recent large European study demonstrated that intake of low glycemic index carbohydrates combined with a modest increase in protein content improved maintenance of weight loss (60). Obviously, increased adipose tissue mass is related to energy-intake. However, as demonstrated here, the macronutrient composition can influence energy efficiency, and mice consuming the same amount of calories end up with quite different amounts of adipose tissue. Of note, increasing the amount of sucrose from 13 to 43% led to an approximately 5-fold higher energy efficiency. Circulating insulin levels may also indirectly influence energy efficiency. Hepatic PGC- 1α is a central target of the insulin/glucagon axis regulating activation of the entire gluconeogenesis cascade in liver (61-63) and a dose-dependent decrease in Ppargc1a and Pck1 expression was observed in response to increasing intake of dietary sucrose. This might be of importance regarding energy efficiency as gluconeogenesis requires ATP and activation of gluconeogenesis reduces feed efficiency as protein is converted to glucose at a cost of 16-20 kJ/g protein (64). Moreover, increased catabolism of amino acids requires ATP for disposal of nitrogen as urea at an energy-cost 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 and 14: high dietary PUFAs, the modulation
Page 15 and 16: In a pair of population studies, an
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: 256 257 258 259 260 261 262 263 264
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
Page 74 and 75: Cyclooxygenases and UCP1 Although i
Page 76 and 77: Cyclooxygenases and UCP1 Figure 2.
Page 78 and 79: Cyclooxygenases and UCP1 Figure 4.
Page 80 and 81: Cyclooxygenases and UCP1 PLoS ONE |
Page 82 and 83: Cyclooxygenases and UCP1 E synthase
Page 84 and 85: Cyclooxygenases and UCP1 29. Granne
Page 86 and 87: JBC Papers in Press. Published on J
Page 88 and 89: hydrolysate (SPH), would be protect
Page 90 and 91: was used as the liver cytosolic fra
Page 92 and 93: In order to demonstrate that bile a
Page 94 and 95: Nutritional regulation of endogenou
Page 96 and 97: in increased whole body energy expe
Page 98 and 99:
38. Kanehisa M, and Goto S. (2000)
Page 100 and 101:
FOOTNOTES This work was carried out
Page 102 and 103:
fed the same diets, plus the SPH-di
Page 104 and 105:
Figure 2 A nmol/ min/ mg prot 2,4 1
Page 106 and 107:
Figure 4 A 6 Liver Pparα B 21 Live
Page 108 and 109:
Figure 7 A Plasma ALAT B Liver Ucp2
Page 110 and 111:
Ruzzin et al. investigated the meta
Page 112 and 113:
Ruzzin et al. CD14, and rho kinases
Page 114 and 115:
Ruzzin et al. salmon oil induced a
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