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Effect of L-Carnitine on Skeletal Muscle Lipids and Oxidative Stress in Rats Fed High-Fructose Diet  [PDF]
Panchamoorthy Rajasekar,Carani Venkatraman Anuradha
Experimental Diabetes Research , 2007, DOI: 10.1155/2007/72741
Abstract: There is evidence that high-fructose diet induces insulin resistance, alterations in lipid metabolism, and oxidative stress in rat tissues. The purpose of this study was to evaluate the effect of L-carnitine (CAR) on lipid accumulation and peroxidative damage in skeletal muscle of rats fed high-fructose diet. Fructose-fed animals (60 g/100 g diet) displayed decreased glucose/insulin (G/I) ratio and insulin sensitivity index (ISI0,120) indicating the development of insulin resistance. Rats showed alterations in the levels of triglycerides, free fatty acids, cholesterol, and phospholipids in skeletal muscle. The condition was associated with oxidative stress as evidenced by the accumulation of lipid peroxidation products, protein carbonyls, and aldehydes along with depletion of both enzymic and nonenzymic antioxidants. Simultaneous intraperitoneal administration of CAR (300 mg/kg/day) to fructose-fed rats alleviated the effects of fructose. These rats showed near-normal levels of the parameters studied. The effects of CAR in this model suggest that CAR supplementation may have some benefits in patients suffering from insulin resistance.
Metabolic responses to acute physical exercise in young rats recovered from fetal protein malnutrition with a fructose-rich diet
Lucieli T Cambri, Gustavo G de Araujo, Ana C Ghezzi, José D Botezelli, Maria AR Mello
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-164
Abstract: Pregnant Wistar rats were fed with a balanced (B) diet or a low-protein (L) diet. After birth and until 60 days of age, the offspring were distributed into four groups according to the diet received: B: B diet during the whole experiment; balanced/fructose (BF): B diet until birth and fructose-rich (F) diet afterwards; low protein/balanced (LB): L diet until birth and B diet afterwards; low protein/fructose (LF): L diet until birth and F diet afterwards.The excess fructose intake reduced the body weight gain, especially in the BF group. Furthermore, the serum total cholesterol and the LDL cholesterol were elevated in this group. In the LF group, the serum total cholesterol and the muscle glycogen increased. Acute physical exercise increased the serum concentrations of glucose, triglycerides, HDL cholesterol and liver lipids and reduced the concentrations of muscle glycogen in all groups.An excess fructose intake induced some signs of metabolic syndrome. However, protein malnutrition appeared to protect against the short term effects of fructose. In other hand, most responses to acute physical exercise were not influenced by early malnutrition and/or by the fructose overload.The worldwide incidence of severe malnutrition has decreased in the last decades. However, malnutrition considered as "mild" or "moderate", associated with anemia of pregnancy, low birth weights and stunted growth in children, is still highly prevalent in third world countries. In 2000, the incidence of children born globally with low birth weight was about 15.5%, with the highest rate (27.1%) observed in South Asia. More than 20 million underweight children are born every year in developing countries [1].Malnutrition in utero can "program" the fetal tissues, making them more vulnerable to disturbances associated with eating, such as type 2 diabetes, metabolic syndrome and other chronic diseases in adulthood [2,3]. Likewise, the excessive consumption of fructose in the diet of contemporary societ
A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats
Bezerra, R.M.N.;Ueno, M.;Silva, M.S.;Tavares, D.Q.;Carvalho, C.R.O.;Saad, M.J.A.;Gontijo, J.A.R.;
Brazilian Journal of Medical and Biological Research , 2001, DOI: 10.1590/S0100-879X2001000900008
Abstract: rats fed a high-fructose diet represent an animal model for insulin resistance and hypertension. we recently showed that a high-fructose diet containing vegetable oil but a normal sodium/potassium ratio induced mild insulin resistance with decreased insulin receptor substrate-1 tyrosine phosphorylation in the liver and muscle of normal rats. in the present study, we examined the mean blood pressure, serum lipid levels and insulin sensitivity by estimating in vivo insulin activity using the 15-min intravenous insulin tolerance test (itt, 0.5 ml of 6 μg insulin, iv) followed by calculation of the rate constant for plasma glucose disappearance (kitt) in male wistar-hannover rats (110-130 g) randomly divided into four diet groups: control, 1:3 sodium/potassium ratio (rna:k) diet (c 1:3 rna:k); control, 1:1 sodium/potassium ratio diet (cna 1:1 rna:k); high-fructose, 1:3 sodium/potassium ratio diet (f 1:3 rna:k), and high-fructose, 1:1 sodium/potassium ratio diet (fna 1:1 rna:k) for 28 days. the change in rna:k for the control and high-fructose diets had no effect on insulin sensitivity measured by itt. in contrast, the 1:1 rna:k increased blood pressure in rats receiving the control and high-fructose diets from 117 ± 3 and 118 ± 3 mmhg to 141 ± 4 and 132 ± 4 mmhg (p<0.05), respectively. triacylglycerol levels were higher in both groups treated with a high-fructose diet when compared to controls (c 1:3 rna:k: 1.2 ± 0.1 mmol/l vs f 1:3 rna:k: 2.3 ± 0.4 mmol/l and cna 1:1 rna:k: 1.2 ± 0.2 mmol/l vs fna 1:1 rna:k: 2.6 ± 0.4 mmol/l, p<0.05). these data suggest that fructose alone does not induce hyperinsulinemia or hypertension in rats fed a normal rna:k diet, whereas an elevation of sodium in the diet may contribute to the elevated blood pressure in this animal model.
A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats  [cached]
Bezerra R.M.N.,Ueno M.,Silva M.S.,Tavares D.Q.
Brazilian Journal of Medical and Biological Research , 2001,
Abstract: Rats fed a high-fructose diet represent an animal model for insulin resistance and hypertension. We recently showed that a high-fructose diet containing vegetable oil but a normal sodium/potassium ratio induced mild insulin resistance with decreased insulin receptor substrate-1 tyrosine phosphorylation in the liver and muscle of normal rats. In the present study, we examined the mean blood pressure, serum lipid levels and insulin sensitivity by estimating in vivo insulin activity using the 15-min intravenous insulin tolerance test (ITT, 0.5 ml of 6 μg insulin, iv) followed by calculation of the rate constant for plasma glucose disappearance (Kitt) in male Wistar-Hannover rats (110-130 g) randomly divided into four diet groups: control, 1:3 sodium/potassium ratio (R Na:K) diet (C 1:3 R Na:K); control, 1:1 sodium/potassium ratio diet (CNa 1:1 R Na:K); high-fructose, 1:3 sodium/potassium ratio diet (F 1:3 R Na:K), and high-fructose, 1:1 sodium/potassium ratio diet (FNa 1:1 R Na:K) for 28 days. The change in R Na:K for the control and high-fructose diets had no effect on insulin sensitivity measured by ITT. In contrast, the 1:1 R Na:K increased blood pressure in rats receiving the control and high-fructose diets from 117 ± 3 and 118 ± 3 mmHg to 141 ± 4 and 132 ± 4 mmHg (P<0.05), respectively. Triacylglycerol levels were higher in both groups treated with a high-fructose diet when compared to controls (C 1:3 R Na:K: 1.2 ± 0.1 mmol/l vs F 1:3 R Na:K: 2.3 ± 0.4 mmol/l and CNa 1:1 R Na:K: 1.2 ± 0.2 mmol/l vs FNa 1:1 R Na:K: 2.6 ± 0.4 mmol/l, P<0.05). These data suggest that fructose alone does not induce hyperinsulinemia or hypertension in rats fed a normal R Na:K diet, whereas an elevation of sodium in the diet may contribute to the elevated blood pressure in this animal model.
Fructose and cardiometabolic disorders: the controversy will, and must, continue
Wiernsperger, Nicolas;Geloen, Alain;Rapin, Jean-Robert;
Clinics , 2010, DOI: 10.1590/S1807-59322010000700013
Abstract: the present review updates the current knowledge on the question of whether high fructose consumption is harmful or not and details new findings which further pushes this old debate. due to large differences in its metabolic handling when compared to glucose, fructose was indeed suggested to be beneficial for the diet of diabetic patients. however its growing industrial use as a sweetener, especially in soft drinks, has focused attention on its potential harmfulness, possibly leading to dyslipidemia, obesity, insulin resistance/metabolic syndrome and even diabetes. many new data have been generated over the last years, confirming the lipogenic effect of fructose as well as risks of vascular dysfunction and hypertension. fructose exerts various direct effects in the liver, affecting both hepatocytes and kupffer cells and resulting in non-alcoholic steatotic hepatitis, a well known precursor of the metabolic syndrome. hepatic metabolic abnormalities underlie indirect peripheral metabolic and vascular disturbances, for which uric acid is possibly the culprit. nevertheless major caveats exist (species, gender, source of fructose, study protocols) which are detailed in this review and presently prevent any firm conclusion. new studies taking into account these confounding factors should be undertaken in order to ascertain whether or not high fructose diet is harmful.
Affective Disorders and Antidepressant Drugs
Marc Fakhoury
Open Access Library Journal (OALib Journal) , 2014, DOI: 10.4236/oalib.1100597
Abstract: Affective disorders are a group of psychiatric diseases that can affect an individual at any given age. Also called mood disorders, they can be distinguished into two different types: major depressive disorder, also called major depression, and bipolar disorder, which is known as manic depression. People affected by major depression most often have a low mood, and are consistently in a state of unhappiness. Although it was shown that genetics play a role in the predisposition of depression, this disease most often occurs in response to a variety of external factors such as a stressful life event, the loss of a loved one, and following drug or substance abuse. A variety of antidepressant drugs, such as the monoamine oxidase inhibitors (MAOIs), the tricyclic antidepressants (TCAs), and the second-generation antidepressants are able to provide significant relief for people suffering from affective disorders like depression. However, several of these pharma- ceutical agents can cause serious side effects to the patients. Therefore, there is a need to identify novel antidepressant therapies that are more efficient and that present minimal side effects. A better understanding of the neurobiology of depression will definitively help scientists develop new therapeutic ideas. This paper will first discuss the clinical profile of depression and explain the physiological mechanisms and the neurochemistry involved in this disease. It will then give you an overview of the effectiveness of the most common antidepressants used, with a description of their mode of action and most notable side effects.
Evaluating of High Fructose Diet to Induce Hyperglycemia and its Inflammatory Complications in Rats
Aida Zarfeshani,Mohd Sokhini Abd Mutalib,Huzwah Khaza`ai
Pakistan Journal of Nutrition , 2012,
Abstract: It has been reported that a diet enriched in fructose would present animal models used to emulate diabetes mellitus type 2 in human. This study aimed to examine the effect of high fructose induction on the blood glucose, C-reactive protein, interleukin-6, interleukin-4 and body weight among high fructose diet-induced rats. The HFD was induced through drinking water in 21% (w/v) concentration among male Sprague-Dawley rats. The high fructose diet administration was unable to induce hyperglycemia, hypertriglyceridemia or any classic inflammatory markers. Also, no histological inflammation was observed. It was concluded that healthy Sprague-Dawley rats fed high fructose diet for 2.5 months could not develop signs of diabetes mellitus type 2.
Circadian polymorphisms associated with affective disorders
Daniel F Kripke, Caroline M Nievergelt, EJ Joo, Tatyana Shekhtman, John R Kelsoe
Journal of Circadian Rhythms , 2009, DOI: 10.1186/1740-3391-7-2
Abstract: Four groups of subjects were recruited from several sources: 1) bipolar proband-parent trios or sib-pair-parent nuclear families, 2) unrelated bipolar participants who had completed the BALM morningness-eveningness questionnaire, 3) sib pairs from the GenRed Project having at least one sib with early-onset recurrent unipolar depression, and 4) a sleep clinic patient group who frequently suffered from depression. Working mainly with the SNPlex assay system, from 2 to 198 polymorphisms in genes related to circadian function were genotyped in the participant groups. Associations with affective disorders were examined with TDT statistics for within-family comparisons. Quantitative trait associations were examined within the unrelated samples.In NR1D1, rs2314339 was associated with bipolar disorder (P = 0.0005). Among the unrelated bipolar participants, 3 SNPs in PER3 and CSNK1E were associated with the BALM score. A PPARGC1B coding SNP, rs7732671, was associated with affective disorder with nominal significance in bipolar family groups and independently in unipolar sib pairs. In TEF, rs738499 was associated with unipolar depression; in a replication study, rs738499 was also associated with the QIDS-SR depression scale in the sleep clinic patient sample.Along with anti-manic effects of lithium and the antidepressant effects of bright light, these findings suggest that perturbations of the circadian gene network at several levels may influence mood disorders, perhaps ultimately through regulation of MAOA and its modulation of dopamine transmission. Twenty-three associations of circadian polymorphisms with affective symptoms met nominal significance criteria (P < 0.05), whereas 15 would be expected by chance, indicating that many represented false discoveries (Type II errors). Some evidence of replication has been gathered, but more studies are needed to ascertain if circadian gene polymorphisms contribute to susceptibility to affective disorders.The idea that circadian rh
Fructose Diet-Induced Skin Collagen Abnormalities Are Prevented by Lipoic Acid  [PDF]
V. Thirunavukkarasu,A. T. Anitha Nandhini,C. V. Anuradha
Experimental Diabetes Research , 2004, DOI: 10.1080/154386090506148
Abstract: Nonenzymatic glycation of proteins, leading to chemical modification and cross-linking are of importance in the pathology of diabetic complications.We studied the effect of α-lipoic acid (LA) on the content and characteristics of the protein collagen from skin of high-fructose fed rats. The rats were divided into 4 groups of 6 each. Two groups of rats were fed with a high fructose diet (60 g/100 g diet) and administered either LA (35 mg/kg b.w., i.p) (FRU+LA) or 0.2 ml vehicle (saline) (FRU) for 45 days. The other 2 groups were fed with control diet containing starch (60 g/100 g diet) and administered either saline (CON) or lipoic acid (CON+LA). The rats were maintained for 45 days and then sacrificed. Plasma glucose, insulin, fructosamine, protein glycation, and blood glycated hemoglobin (HbA1C) were measured. Collagen was isolated from skin and the physicochemical properties of collagen were studied. Fructose administration caused accumulation of collagen in skin. Extensive cross-linking was evidenced by enhanced glycation and AGE-linked fluorescence. Increased peroxidation and changes in physicochemical properties such as shrinkage temperature, aldehyde content, solubililty pattern, susceptibility to denaturing agents were observed in fructose-fed rats. SDS gel pattern of collagen from these rats showed elevated β component of type I collagen. These changes were alleviated by the simultaneous administration of LA. Administration of LA to fructose-fed rats had a positive influence on both quantitative and qualitative properties of collagen. The results suggest a mechanism for the ability of LA to delay diabetic complications.
Oral Metformin Treatment Prevents Enhanced Insulin Demand and Placental Dysfunction in the Pregnant Rat Fed a Fructose-Rich Diet  [PDF]
Ana Alzamendi,Hector Del Zotto,Daniel Castrogiovanni,Jose Romero,Andres Giovambattista,Eduardo Spinedi
ISRN Endocrinology , 2012, DOI: 10.5402/2012/757913
Abstract: The intake of a fructose-rich diet (FRD) in the normal female rat induces features similar to those observed in the human metabolic syndrome phenotype. We studied the impact of FRD administration to mothers on pregnancy outcome. On gestational day (Gd) zero rats were assigned to either group: ad libitum drinking tap water alone (normal diet, ND) or containing fructose (10% w/vol; FRD) through pregnancy; all rats were fed a Purina chow diet ad libitum ND and FRD rats were daily cotreated or not with metformin (60?mg/Kg/day oral; ND + MF and FRD + MF) and submitted to a high glucose load test on Gd 14. Additionally, placentas from different groups were studied on Gd 20. Data indicated that: (1) although FRD rats well tolerated glucose overload, their circulating levels of insulin were significantly higher than in ND rats; (2) the mesometrial triangle blood vessel area was significantly lower in placentas from FRD than ND dams; (3) the detrimental effects of FRD administration to mothers were ameliorated by metformin cotreatment. Our study suggests that excessive intake of fructose during pregnancy enhanced the risk for developing gestational diabetes and subsequent preeclampsia, and that metformin prevented the poor pregnancy outcome induced by FRD. 1. Introduction The prevalence of gestational diabetes mellitus (GDM) has significantly increased during the last decades [1], and offspring born to mothers with GDM present a significantly increased risk of developing obesity and type 2 diabetes mellitus (T2DM) [2, 3]. Maternal anthropometric factors (e.g., prepregnancy body weight (BW), adiposity weight gain during pregnancy) account for the variance in offspring BW and adiposity at birth [1, 4], and on other risk factors as well [5, 6]. However, maternal nutrition is a highly important conditioning factor of fetal growth. GDM is characterized by impaired glucose tolerance/decreased insulin sensitivity, and mothers with GDM have an increased risk of developing preeclampsia (PE) [7, 8]. Although the pathogenesis of PE still remains unclear, it is accepted that PE is an endothelial cell disorder associated with marked maternal and neonatal morbidity [9]. On the other hand, insulin effectiveness and angiogenesis [10–12] are key factors for the control of endothelial cell function. Consequently, the presence of decreased insulin sensitivity in the mother may enhance the defects in angiogenic function [13, 14], leading to an increased risk of PE. Maternal nutritional disturbances during critical developmental periods [15–17] are known to raise the offspring’s
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