Because complications from obesity such as diabetes and cardiovascular disease usually require decades, surrogate animal models are important for studying the molecular aspects of obesity and its pathophysiological effects.
Heat treatment improves glucose tolerance and prevents skeletal muscle insulin resistance in rats fed a high-fat diet. Data from L6 cells suggest that one bout of heat treatment increases mitochondrial oxygen consumption and fatty acid oxidation.
He naturally wanted to find an explanation for the dramatically different effects the diet had on rodents and humans. High fat diet damages human foetuses The release then goes on unhesitatingly to declare that the human foetus would be harmed by high fat in the same way.
Shown are exemplary studies highlighting the range of changes observed. Rodent high fat studies deeply misleading Grapefruit juice may or may not help obese and diabetic humans; a good way to find out would be to give it to humans in a trial. Our results indicate that heat treatment protects skeletal muscle from high-fat diet-induced insulin resistance and provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for obesity-induced insulin resistance.
No significant associations could be detected.
With special thanks to Peter Dobromylskyj a vet with physiology degree, who runs a very sophisticated academic blog on diet and health at http: The phenotypic variations between these two inbred strains might be due to an altered hypothalamic gene expression 26leptin sensitivity 27sympathetic stimulation 28or epigenetic programming Adipokines Adipokines such as leptin, adiponectin, or resistin are recognized as systemic factors influencing insulin sensitivity.
This model has lead to many discoveries of the important signalings in obesity, such as Akt and mTOR. There was no attempt to suggest that the reaction of rodents might be different to that of humans — a basic caveat with any animal research. Body weight gain during the feeding period is gradual Figure 1.
Mitochondrial citrate synthase and cytochrome oxidase activity decreased slightly with the high-fat diet, but heat treatment restored these activities. Human insulin: In fact it seems the rodent work is highly misleading. Recent studies have shown that S6K1-deficient mice and Akt1 knockout mice exhibit are prevented from diet-induced obesity through model of murine high-fat diet induced obesity described below Meanwhile the sugar in the high fat diet is linked to weight gain and insulin resistance.
Until then, before swallowing any rodent high fat result, season it with a large pinch of salt. Data on total cholesterol levels under HF diets are inconsistent, and definite statements about the putative induction of hypercholesterinemia by a pure HF diet, i.
Epub Dec This dubious mixture is then fed to animals that are unlike any found in nature as they have been selected for fat sensitivity; one widely used variant puts on weight and develops raised insulin even when being fed zero carbohydrates!
These include weight loss with no cut in calories, increased energy, improved glucose tolerance and reduced insulin. Inclusion criteria were: A useful start to correct it would be for all studies to make clear what the high fat diet actually consisted of and what strain of specially selected rodent was being used and what it had been selected for.Nevertheless, the full manifested picture of obesity develops after 16 weeks of high-fat diet with adipocyte hyperplasia, fat deposition in mesentery, increased fat mass, diabetes, and hypertension.
Akt and mTOR pathyway integrates several important signals that regulate cell growth and robadarocker.com by: Heat treatment improves glucose tolerance and prevents skeletal muscle insulin resistance in rats fed a high-fat diet.
Gupte AA(1), Bomhoff GL, Swerdlow RH, Geiger PC. Author information: (1)Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, robadarocker.com by: Wenche Jørgensen, Kasper A. Rud, Ole H. Mortensen, Lis Frandsen, Niels Grunnet and Bjørn Quistorff, Your mitochondria are what you eat: a high‐fat or a high‐sucrose diet eliminates metabolic flexibility in isolated mitochondria from rat skeletal muscle, Physiological Reports, 5, 6, ().Cited by: Rats need: Fresh/healthy/balanced diets meeting their nutritional needs; easily achieved by feeding balanced commercial pelleted diets especially for rats.
Occasional variety. Consider supplementing diets with small amounts of fruit/vegetables/cooked egg/grains/seeds, given as part of their daily ration, not in addition or it could cause obesity/health problems.
Rats are omnivores eating both plant and animal. Not only are the so called ‘high fat diets’ they are fed nothing like the low carbohydrate diets any informed human would follow, but the animals have been selectively bred to ensure they become fat and diabetic on a high fat diet.
This is not research, it is a rigged game.