Palmitate and glucose oxidation by diaphragm of rats with fructose-induced hypertriglyceridemia

Vrána, A.; Fábry, P.; Kazdová, Ludmila

doi:10.1016/0026-0495(78)90131-2

Cited by 31 publications

(15 citation statements)

References 10 publications

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“…14 C]glucose to [ 14 C]glycogen) was determined in isolated soleus muscle, as described previously (34,44,46).…”

Section: Methodsmentioning

confidence: 99%

“…In short, after decapitation, distal parts of the epididymal adipose tissue (200 mg) were incubated in KrebsRinger bicarbonate buffer, as described previously (34,44,46). Total adipose tissue lipids were extracted according to Folch et al (10), and the radioactivity was determined as described previously (44).…”

Section: Insulin-stimulated Lipogenesis Basal and Insulin-stimulatedmentioning

confidence: 99%

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Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

Šedová¹,

Šeda²,

Kazdová³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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-The importance of early environment, including maternal diet during pregnancy, is suspected to play a major role in pathogenesis of metabolic syndrome and related conditions. One of the proposed mechanisms is a mismatch between the prenatal and postnatal environments, leading to misprogramming of the metabolic and signaling pathways of the developing fetus. We assessed whether the exposure to high-sucrose diet (HSD) alleviates the detrimental effects of sucrose feeding in later life (predictive adaptive hypothesis) in a highly inbred model of metabolic syndrome, the PD/Cub rat. Rat dams were continuously fed either standard or HSD (70% calories as sucrose) starting 1 wk before breeding, throughout pregnancy, at birth, and until weaning of the offspring. After weaning, all male offspring were fed HSD until the age of 20 wk, when detailed metabolic and morphometric profiles were ascertained. The early life exposure to a sucrose-rich diet resulted in distinct responses to longtime postnatal HSD feeding. Offspring of the sucrose-fed mothers displayed higher adiposity and substantial increases in triglyceride liver content together with unfavorable distribution of cholesterol into lipoprotein subfractions. On the other hand, their adiponectin concentrations were significantly higher, and insulin sensitivity of skeletal muscle was enhanced compared with the offspring of standard diet-fed mothers. Triglycerides, free fatty acids, overall glucose tolerance, and the insulin sensitivity of adipose tissue were comparable in both groups. In the genetically identical animals, maternal HSD feeding elicited a variety of subtle effects but did not lead to predictive adaptive protection from most HSD-induced metabolic derangements. developmental plasticity; animal model; PD/Cub; maternal diet GROWING EVIDENCE SUGGESTS that fetal and early life environment are determinants of disease in adult life, including dyslipidemia, insulin resistance, obesity, and hypertension (1, 26). The "thrifty phenotype" hypothesis (2) confronted the 30-yrolder "thrifty genotype" concept (28), which linked the manifestations of cardiovascular disease, insulin resistance, and diabetes in adulthood with fetal malnutrition rather than with modulation of metabolic and signaling pathways by environ-

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“…14 C]glucose to [ 14 C]glycogen) was determined in isolated soleus muscle, as described previously (34,44,46).…”

Section: Methodsmentioning

confidence: 99%

Section: Insulin-stimulated Lipogenesis Basal and Insulin-stimulatedmentioning

confidence: 99%

Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

Šedová¹,

Šeda²,

Kazdová³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…We drew blood from the tail without anesthesia for measurements of glucose, insulin, and triglycerides as previously described (Pravenec et al 2003). We obtained samples of gastrocnemius muscle by snap-freezing in liquid nitrogen and measured glycogen content enzymatically as glucose using the glucose oxidase method in chloroformmethanol sediment after acid hydrolysis as previously described (Vrana et al 1978). We also processed snap-frozen samples of gastrocnemius muscle in liquid nitrogen for measurement of ATP content by high-pressure liquid chromatography as previously described (Flachs et al 2002).…”

Section: Risk Factor Phenotypingmentioning

confidence: 99%

Direct linkage of mitochondrial genome variation to risk factors for type 2 diabetes in conplastic strains

Pravenec¹,

Hyakukoku

Houštěk³

et al. 2007

Genome Res.

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Recently, the relationship of mitochondrial DNA (mtDNA) variants to metabolic risk factors for diabetes and other common diseases has begun to attract increasing attention. However, progress in this area has been limited because (1) the phenotypic effects of variation in the mitochondrial genome are difficult to isolate owing to confounding variation in the nuclear genome, imprinting phenomena, and environmental factors; and (2) few animal models have been available for directly investigating the effects of mtDNA variants on complex metabolic phenotypes in vivo. Substitution of different mitochondrial genomes on the same nuclear genetic background in conplastic strains provides a way to unambiguously isolate effects of the mitochondrial genome on complex traits. Here we show that conplastic strains of rats with identical nuclear genomes but divergent mitochondrial genomes that encode amino acid differences in proteins of oxidative phosphorylation exhibit differences in major metabolic risk factors for type 2 diabetes. These results (1) provide the first direct evidence linking naturally occurring variation in the mitochondrial genome, independent of variation in the nuclear genome and other confounding factors, to inherited variation in known risk factors for type 2 diabetes; and (2) establish that spontaneous variation in the mitochondrial genome per se can promote systemic metabolic disturbances relevant to the pathogenesis of common diseases.[Supplemental material is available online at www.genome.org.]Recently, the potential role of the mitochondrial genome in the pathogenesis of type 2 diabetes and other common diseases has begun to attract increasing attention (Wallace 2005). Mitochondrial DNA is exclusively of maternal origin, and some studies have indicated that the inheritance of type 2 diabetes may be biased toward the maternal lineage (Alcolado et al. 2002). Sun et al. (2003) have estimated that mitochondrial DNA mutations might be involved in >20% of cases of type 2 diabetes. In addition, Wilson et al. (2004) have identified a homoplasmic mitochondrial DNA variant associated with the maternal transmission of hypercholesterolemia, hypomagnesemia, and hypertension through four generations of a large, carefully analyzed kindred. Rare forms of maternally transmitted diabetes associated with heteroplasmic mitochondrial DNA variants have also been reported (Mathews and Berdanier 1998;Maassen et al. 2005). These observations provide indirect evidence that sequence variation in the mitochondrial genome might contribute to inherited variation in the risk for type 2 diabetes and related metabolic disorders.Notwithstanding recent advances in mitochondrial genome research, multiple confounding factors have made it difficult to unequivocally establish a role for mitochondrial DNA variation in the regulation of risk factors for diabetes or other complex metabolic phenotypes. For example, effects of maternal environment or imprinting may contribute to matrilineal transmission patterns of the phenotypes of interest....

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“…Similarly, Vrana et al 14 ) and Kannan et alY) showed that the enzyme activity in the adipose tissue of rats fed a glucose diet was similar to that in animals fed on a fructose diet.…”

mentioning

confidence: 78%

Effects of Dietary Fructose, Glucose, Fibers and Hypolipidemic Drugs on Serum and Liver Lipids in Rats

Aoyama

Otaki

Yoshino

et al. 1987

Agricultural and Biological Chemistry

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Palmitate and glucose oxidation by diaphragm of rats with fructose-induced hypertriglyceridemia

Cited by 31 publications

References 10 publications

Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

Sucrose feeding during pregnancy and lactation elicits distinct metabolic response in offspring of an inbred genetic model of metabolic syndrome

Direct linkage of mitochondrial genome variation to risk factors for type 2 diabetes in conplastic strains

Effects of Dietary Fructose, Glucose, Fibers and Hypolipidemic Drugs on Serum and Liver Lipids in Rats

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