scholarly journals The metabolic syndrome of fructose-fed rats: Effects of long-chain polyunsaturated ω3 and ω6 fatty acids. II. Time course of changes in food intake, body weight, plasma glucose and insulin concentrations and insulin resistance

Author(s):  
Willy Malaisse
Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1438
Author(s):  
Rola Hammoud ◽  
Emanuela Pannia ◽  
Ruslan Kubant ◽  
Adam Metherel ◽  
Rebecca Simonian ◽  
...  

Maternal choline intakes are below recommendations, potentially impairing the child’s later-life metabolic health. This study aims to elucidate the interaction between the choline content of the gestational diet (GD) and fat content of the post-weaning diet (PWD) on metabolic phenotype of male Wistar rats. Pregnant Wistar rats were fed a standard rodent diet (AIN-93G) with either recommended choline (RC, 1 g/kg diet choline bitartrate) or high choline (HC, 2.5-fold). Male pups were weaned to either a normal (16%) fat (NF) or a high (45%) fat (HF) diet for 17 weeks. Body weight, visceral adiposity, food intake, energy expenditure, plasma hormones, triglycerides, and hepatic fatty acids were measured. HC-HF offspring had 7% lower body weight but not food intake, and lower adiposity, plasma triglycerides, and insulin resistance compared to RC-HF. They also had increased hepatic n-3 fatty acids and a reduced n-6/n-3 and C 18:1 n-9/C18:0 ratios. In contrast, HC-NF offspring had 6–8% higher cumulative food intake and body weight, as well as increased leptin and elevated hepatic C16:1 n-7/C16:0 ratio compared to RC-NF. Therefore, gestational choline supplementation associated with improved long-term regulation of several biomarkers of the metabolic syndrome in male Wistar rat offspring fed a HF, but not a NF, PWD.


2005 ◽  
Vol 64 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Helen M. Roche

The metabolic syndrome is a very common condition, characterised by insulin resistance, dyslipidaemia, abdominal obesity and hypertension, that is associated with a high risk of type 2 diabetes mellitus (T2DM) and CVD. Obesity is a key aetiological factor in the development of the metabolic syndrome. In light of the increasing prevalence of obesity, there is a high requirement to reduce the impact of the adverse health effects associated with the metabolic syndrome. The aetiological role of nutrient-derived metabolic stressors, in particular fatty acids, in the development of obesity and the metabolic syndrome is explored. Also, the evidence that pro-inflammatory stressors may predispose to obesity-induced insulin resistance is reviewed. The present paper explores the concept that reducing the impact of metabolic and inflammatory stressors may reduce the adverse health effects of obesity and slow the progression towards the metabolic syndrome and T2DM. Evidence from human dietary intervention studies that have investigated the potential therapeutic effects of dietary fatty acid modification is explored. The present review highlights the requirement to take account of genetic background, within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. This approach will further the understanding of the interaction between fatty acids in the pathogenesis and progression of the metabolic syndrome.


2013 ◽  
Vol 10 (1) ◽  
pp. 27-38 ◽  
Author(s):  
Christina Chrysohoou ◽  
Demosthenes Panagiotakos ◽  
Christos Pitsavos ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
...  

2012 ◽  
Vol 6 (6) ◽  
pp. 1404-1408 ◽  
Author(s):  
ZOHEIR MELLOUK ◽  
EMELINE HUPKENS ◽  
MARIE-HELENE ANTOINE ◽  
ABDULLAH SENER ◽  
DALILA AIT YAHIA ◽  
...  

2010 ◽  
Vol 69 (3) ◽  
pp. 324-332 ◽  
Author(s):  
María J. Moreno-Aliaga ◽  
Silvia Lorente-Cebrián ◽  
J. Alfredo Martínez

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. Then-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact,n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability ofn-3 PUFA to regulate adipokine gene expression and secretion has been observed bothin vitroandin vivoin rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions ofn-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability ofn-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.


2012 ◽  
Vol 6 (6) ◽  
pp. 1399-1403 ◽  
Author(s):  
ZOHEIR MELLOUK ◽  
KARIM LOUCHAMI ◽  
EMELINE HUPKENS ◽  
ABDULLAH SENER ◽  
DALILA AIT YAHIA ◽  
...  

1998 ◽  
Vol 84 (4) ◽  
pp. 1311-1315 ◽  
Author(s):  
R. James Barnard ◽  
Christian K. Roberts ◽  
Shira M. Varon ◽  
Joshua J. Berger

This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.


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