Effects of dietary glucose or fructose on the secretion rate and particle size of triglyceride-rich lipoproteins in Zucker fatty rats

Kazumi, Tsutomu; Yoshino, Gen; Matsuba, Kohji; Iwai, Masahide; Iwatani, Ippei; Matsushita, Masayuki; Kasama, Toshio; Hosokawa, Tomoyoshi; Numano, Fujío; Baba, Shigeaki

doi:10.1016/0026-0495(91)90073-6

Cited by 17 publications

(6 citation statements)

References 22 publications

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“…This was associated with greater hepatic activities of fatty acid synthetase and NADPH-generating enzymes, as previously reported [18,19]. In the present study, the rate of triglyceride secretion averaged 16.2 umol/min in Wistar fatty control rats and this figure was comparable to the rate of triglyceride secretion in Zucker fatty rats [4,8]. The Triton method is reproducible and reliable when it is used for comparison between different diets or genotypes, although it probably does not provide absolute values for the rate of lipoprotein production.…”

Section: Discussionsupporting

confidence: 91%

“…We have previously shown that neither fructose nor glucose supplementation produced significant changes in the rate of triglyceride secretion in Zucker fatty rats [4]. Since the previous study using the perfused liver [20] demonstrated that a major portion of the increased triglyceride secretion by the livers from Zucker fatty rats was derived from endogenous rather than exogenous sources, it is likely, as we previously suggested [4], that fructose is not readily converted to fat in Zucker fatty rat livers.…”

Section: Discussionmentioning

confidence: 88%

“…Since the previous study using the perfused liver [20] demonstrated that a major portion of the increased triglyceride secretion by the livers from Zucker fatty rats was derived from endogenous rather than exogenous sources, it is likely, as we previously suggested [4], that fructose is not readily converted to fat in Zucker fatty rat livers. In contrast to Zucker fatty rats, in Wistar fatty rats, both dietary fructose and glucose stimulated triglyceride production in the present studies.…”

Section: Discussionmentioning

confidence: 91%

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Effects of Dietary Fructose or Glucose on Triglyceride Production and Lipogenic Enzyme Activities in the Liver of Wistar Fatty Rats, an Animal Model of NIDDM.

et al. 1997

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Abstract.Effects of dietary carbohydrates on triglyceride production and hepatic lipogenic enzyme activities were examined in Wistar fatty rats, an animal model of noninsulin dependent diabetes mellitus, fed fructose or glucose and were compared with those of Wistar lean rats. Carbohydrates were supplied in 10% drinking solutions for 21 days. As compared with lean rats, Wistar fatty rats were characterized by hyperglycemia, hyperinsulinemia and hypertriglyceridemia,

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 91%

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Effects of Dietary Fructose or Glucose on Triglyceride Production and Lipogenic Enzyme Activities in the Liver of Wistar Fatty Rats, an Animal Model of NIDDM.

et al. 1997

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“…This may be associated with obesity, hyperphagia, and hyperinsulinemia in Wistar fatty rats. TG secretion rates averaged 16.2 ± 0.1 fxmol/min in fatty rats receiving no fructose feeding, and this figure was comparable to the rate of secretion obtained by the Triton method in Zucker fatty rats (7). Although TG production rates would be underestimated in the Triton method (28), it is nevertheless reproducible and reliable when it is used for comparisons between different genotypes or diets.…”

Section: Discussionmentioning

confidence: 72%

“…We have previously shown that feeding fructose to rodents produced an elevation of plasma triglyceride (TG) in diabetic (4,5) and nondiabetic rats (6,7) and that this was associated not only with an increase in the secretion of VLDL-TG from the liver (6,7) but also with defects in VLDL-TG catabolism from the circulation (4,5,8,9).…”

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confidence: 99%

VLDL Triglyceride Kinetics in Wistar Fatty Rats, An Animal Model of NIDDM: Effects of Dietary Fructose Alone or in Combination With Pioglitazone

Kazumi

Hirano²,

Odaka³

et al. 1996

Diabetes

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The effects of dietary fructose alone or in combination with a new oral agent, pioglitazone, on VLDL-triglyceride (TG) turnover were studied in genetically obese Wistar fatty rats characterized by hyperinsulinemia (7,488 +/- 954 pmol/l), hyperglycemia, (22.5 +/- 1.4 mmol/l), and hypertriglyceridemia (4.39 +/- 0.54 mmol/l). They had an increased hepatic TG production (16.2 +/- 0.1 micromol/min; lean rats, 5.4 +/- 0.3 micromol/min) as well as a longer half-life of VLDL-TG from lean donors (8.8 +/- 1.4 min, lean recipients; 2.3 +/- 0.9 min). In addition, in lean recipients, the half-life of VLDL-TG from fatty donors was longer than that from lean donors (4.80 +/- 0.56 vs. 3.14 +/- 0.23 min). Although feeding fructose into fatty rats did not change plasma glucose and insulin levels, it produced a twofold increase in TG levels (8.74 +/- 1.15 mmol/l). This was associated with a 1.7-fold increase in TG production to 27.5 +/- 1.2 micromol/min, while no significant change was found in the half-life of lean VLDL-TG in fructose-fed fatty recipients (10.9 +/- 2.4 min) or in that of VLDL-TG from fructose-fed fatty donors in lean recipients (4.46 +/- 0.76 min). Daily administration of pioglitazone (3 mg/kg body weight) in fructose-fed fatty rats ameliorated glycemia and triglyceridemia to the level of lean rats (8.1 +/- 0.7 and 1.18 +/- 0.05 mmol/l, respectively) and insulinemia to a lesser extent (2,712 +/- 78 pmol/l). A fall in TG levels was associated with improvement of an impairment in the ability of fructose-fed fatty rats to remove lean VLDL-TG (half-fife: 2.6 +/- 0.6 min). Pioglitazone, however, produced no change in TG production (25.9 +/- 2.7 micromol/min), the half-life of VLDL-TG from fructose-fed fatty donors in lean recipients (4.17 +/- 0.38 min), or the activity of lipoprotein lipase and hepatic lipase in postheparin plasma. We conclude that in Wistar fatty rats 1) hypertriglyceridemia is attributed to TG overproduction and impaired TG catabolism, and the latter is due to changes in both VLDL, such that they are less able to be removed, and changes in the nature of Wistar fatty rats, such that they are less able to remove VLDL-TG; 2) fructose further increases hepatic TG production with a resultant deterioration in hypertriglyceridemia; 3) pioglitazone normalizes TG levels by altering the physiology of the Wistar fatty rats in a manner that increases their ability to remove VLDL-TG from the circulation.

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Animal models of non‐insulin‐dependent diabetes

Shafrir

1992

Diabetes Metab. Rev.

159

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Effects of dietary glucose or fructose on the secretion rate and particle size of triglyceride-rich lipoproteins in Zucker fatty rats

Cited by 17 publications

References 22 publications

Effects of Dietary Fructose or Glucose on Triglyceride Production and Lipogenic Enzyme Activities in the Liver of Wistar Fatty Rats, an Animal Model of NIDDM.

Effects of Dietary Fructose or Glucose on Triglyceride Production and Lipogenic Enzyme Activities in the Liver of Wistar Fatty Rats, an Animal Model of NIDDM.

VLDL Triglyceride Kinetics in Wistar Fatty Rats, An Animal Model of NIDDM: Effects of Dietary Fructose Alone or in Combination With Pioglitazone

Animal models of non‐insulin‐dependent diabetes

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