Wenche Jørgensen

IT University of Copenhagen, København, Capital Region, Denmark

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Publications (6)21.43 Total impact

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    ABSTRACT: Obesity and consumption of a high fat diet are risk factors for the metabolic syndrome and is thought to confer changes in skeletal muscle mitochondrial function. Taurine supplementation has been shown to be able to counteract at least part of the metabolic changes induced by consumption of a high fat diet, yet little is known about the effect of taurine supplementation upon mitochondrial function. Here we assessed the effect of taurine supplementation on glucose and lipid parameters as well as skeletal muscle mitochondrial function in a high fat diet rat model. Male Wistar rats were fed either a control diet, a high fat diet or a high fat diet with taurine supplementation (2 % in the drinking water) for 12 weeks. High fat diet caused an increase in body weight and a marked glucose intolerance. Taurine had no effect on body weight or glucose tolerance. We saw no difference between groups with regard to fasting plasma glucose, free fatty acids or triglycerides or skeletal muscle triglyceride content. However, high fat diet resulted in a marked increase in hepatic triglyceride content, which was counteracted by taurine. High fat diet increased liver, but not skeletal muscle or plasma taurine concentration. Taurine caused an increase in plasma, liver and skeletal muscle taurine concentration. High fat diet increased state 3 respiration in skeletal muscle when using pyruvate as substrate, with no effect of taurine. In conclusion, taurine counteracted a subset of parameters changed by the high fat diet, but had no effect on mitochondrial function.
    No preview · Article · Apr 2015 · Advances in Experimental Medicine and Biology
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    ABSTRACT: We have developed a sheep model to facilitate studies of the fetal programming effects of mismatched perinatal and postnatal nutrition. During the last trimester of gestation, twenty-one twin-bearing ewes were fed a normal diet fulfilling norms for energy and protein (NORM) or 50 % of a normal diet (LOW). From day 3 postpartum to 6 months (around puberty) of age, one twin lamb was fed a conventional (CONV) diet and the other a high-carbohydrate-high-fat (HCHF) diet, resulting in four groups of offspring: NORM-CONV; NORM-HCHF; LOW-CONV; LOW-HCHF. At 6 months of age, half of the lambs (all males and three females) were slaughtered for further examination and the other half (females only) were transferred to a moderate sheep diet until slaughtered at 24 months of age (adulthood). Maternal undernutrition during late gestation reduced the birth weight of LOW offspring (P < 0·05), and its long-term effects were increased adrenal size in male lambs and adult females (P < 0·05), increased neonatal appetite for fat-(P = 0·004) rather than carbohydrate-rich feeds (P < 0·001) and reduced deposition of subcutaneous fat in both sexes (P < 0·05). Furthermore, LOW-HCHF female lambs had markedly higher visceral:subcutaneous fat ratios compared with the other groups (P < 0·001). Postnatal overfeeding (HCHF) resulted in obesity (>30 % fat in soft tissue) and widespread ectopic lipid deposition. In conclusion, our sheep model revealed strong pre- and postnatal impacts on growth, food preferences and fat deposition patterns. The present findings support a role for subcutaneous adipose tissue in the development of visceral adiposity, which in humans is known to precede the development of the metabolic syndrome in human adults.
    Full-text · Article · Oct 2012 · The British journal of nutrition
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    ABSTRACT: Impaired mitochondrial function is implicated in the development of type 2 diabetes mellitus (T2DM). This was investigated in mitochondria from skeletal muscle and liver of the Goto-Kakizaki (GK) rat, which spontaneously develops T2DM with age. The early and the manifest stage of T2DM was studied in 6- and 16-wk-old GK rats, respectively. In GK16 compared with GK6 animals, a decrease in state 3 respiration with palmitoyl carnitine (PC) as substrate was observed in muscle. Yet an increase was seen in liver. To test the complex II contribution to the state 3 respiration, succinate was added together with PC. In liver mitochondria, this resulted in an ∼50% smaller respiratory increase in the GK6 group compared with control and no respiratory increase at all in the GK16 animals. Yet no difference between groups was seen in muscle mitochondria. RCR and P/O ratio was increased (P < 0.05) in liver but unchanged in muscle in both GK groups. We observed increased lipid peroxidation and decreased Akt phosphorylation in liver with the progression of T2DM but no change in muscle. We conclude that, during the progression of T2DM in GK rats, liver mitochondria are affected earlier and/or more severely than muscle mitochondria. Succinate dehydrogenase flux in the presence of fatty acids was reduced severely in liver but not in muscle mitochondria during manifest T2DM. The observations support the notion that T2DM pathogenesis is initiated in the liver and that only later are muscle mitochondria affected.
    Full-text · Article · Jun 2012 · AJP Endocrinology and Metabolism
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    ABSTRACT: In a sheep model, we investigated diet effects on skeletal muscle mitochondria to look for fetal programming. During pregnancy, ewes were fed normally (N) or were 50% food restricted (L) during the last trimester, and lambs born to these ewes received a normal (N) or a high-fat diet (H) for the first 6 mo of life. We examined mitochondrial function in permeabilized muscle fibers from the lambs at 6 mo of age (adolescence) and after 24 mo of age (adulthood). The postpartum H diet for the lambs induced an approximately 30% increase (P < 0.05) of mitochondrial VO(2max) and an approximately 50% increase (P < 0.05) of the respiratory coupling ratio (RCR) combined with lower levels of UCP3 and PGC-1alpha mRNA levels (P < 0.05). These effects proved to be reversible by a normal diet from 6 to 24 mo of age. However, at 24 mo, a long-term effect of the maternal gestational diet restriction (fetal programming) became evident as a lower VO(2max) (approximately 40%, P < 0.05), a lower state 4 respiration (approximately 40%, P < 0.05), and lower RCR ( approximately 15%, P < 0.05). Both PGC-1alpha and UCP3 mRNA levels were increased (P < 0.05). Two analyzed muscles were affected differently, and muscle rich in type I fibers was more susceptible to fetal programming. We conclude that fetal programming, seen as a reduced VO(2max) in adulthood, results from gestational undernutrition. Postnatal high-fat diet results in a pronounced RCR and VO(2max) increase in adolescence. However, these effects are reversible by diet correction and are not maintained in adulthood.
    Full-text · Article · Oct 2009 · AJP Endocrinology and Metabolism
  • Lee Stanyer · Wenche Jorgensen · Osamu Hori · John B Clark · Simon J.R. Heales
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    ABSTRACT: The accumulation of oxidatively modified proteins has been shown to be a characteristic feature of many neurodegenerative disorders and its regulation requires efficient proteolytic processing. One component of the mitochondrial proteolytic system is Lon, an ATP-dependent protease that has been shown to degrade oxidatively modified aconitase in vitro and may thus play a role in defending against the accumulation of oxidized matrix proteins in mitochondria. Using an assay system that allowed us to distinguish between basal and ATP-stimulated Lon protease activity, we have shown in isolated non-synaptic rat brain mitochondria that Lon protease is highly susceptible to oxidative inactivation by peroxynitrite (ONOO(-)). This susceptibility was more pronounced with regard to ATP-stimulated activity, which was inhibited by 75% in the presence of a bolus addition of 1mM ONOO(-), whereas basal unstimulated activity was inhibited by 45%. Treatment of mitochondria with a range of peroxynitrite concentrations (10-1000 microM) revealed that a decline in Lon protease activity preceded electron transport chain (ETC) dysfunction (complex I, II-III and IV) and that ATP-stimulated activity was approximately fivefold more sensitive than basal Lon protease activity. Furthermore, supplementation of mitochondrial matrix extracts with reduced glutathione, following ONOO(-) exposure, resulted in partial restoration of basal and ATP-stimulated activity, thus suggesting possible redox regulation of this enzyme complex. Taken together these findings suggest that Lon protease may be particularly vulnerable to inactivation in conditions associated with GSH depletion and elevated oxidative stress.
    No preview · Article · Jul 2008 · Neurochemistry International

  • No preview · Article · Jul 2008 · Biochimica et Biophysica Acta (BBA) - Bioenergetics