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Diet induced obese rat model: High-fat diet-induced obesity Rat model: a comparison between Wistar and Sprague-Dawley Rat

Kaul, and P. Placing diabetic rats on a normal diet or treating them with enalapril or menhaden oil enriched diet lowered serum lipid levels compared to untreated diabetic rats.

Liam Adams
Wednesday, September 4, 2019
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  • Article PubMed Google Scholar 3. Interestingly, platelet levels of the active form of Src pTyr showed a tendency to increase in DIO rats pointing towards a potential dysfunction in Src family kinases-related signalling pathways in obesity.

  • Rats were fed a high fat diet and treated with a low dose of streptozotocin to create models of diet induced obesity or type 2 diabetes, respectively. Jackson, M.

  • Molecular and Cellular Endocrinology 10 — Despite the known link between obesity and postmenopausal breast cancer, the mechanisms underlying this association are not fully understood.

REVIEW article

Oltman, and M. View raw image Circadian rhythm of insulin and leptin at 3, 6, and 9 months of age in free-feeding animals. All diabetic rats were hyperglycemic and this was not affected by treatments.

Relative circulating estrogen levels across the obese rat D1—E and corresponding follicular and luteal phases of the human menstrual cycle are indicated. Indeed, as mentioned above, our group has recently showed moodel platelets from obese patients have higher GPVI surface levels and higher platelet aggregation in response to collagen-related peptide CRP and collagen 9. Replacement of breeding pairs, mainly breeding mothers, has been kept to a minimum. Even in the current obesogenic environment, not all individuals become obese. Using this criteria resulted in a clean separation into obese and lean phenotypes in the mature animals studied between 20 and 30 weeks of agein which obese rats had significantly higher body weight, body fat, and circulating triglycerides when compared to their lean counterparts. Methodology The search for articles was carried out manually on PubMed database by a single researcher in February

Beiswenger, N. Plasma leptin concentrations were also measured. S5—S11, Davidson, A. However, the neuropathic endpoints were not improved. Rats fed a high fat diet do not become hyperglycemic, presumably due to compensatory hyperinsulinemia [ 21 ].

MeSH terms

Oltman, E. Vague, G. Placing diabetic rats on a normal diet and to a greater extent treating diabetic rats with enalapril or a diet enriched with menhaden oil improved intraepidermal nerve fiber density.

Data Brief 23 J Physiol Biochem. Body mass index and risk of breast cancer: a nonlinear dose-response meta-analysis of prospective studies. Pomegranate extract and exercise provide additive benefits on improvement of imune function by inhibiting inflammation and oxidative stress in high-fat-diet-induced obesity in rats.

Henriksen and M. This suggests that an effective treatment for peripheral neuropathy associated with either prediabetes or diabetes is needed and to be efficacious will diet induced obese rat model require early detection followed by a combination of lifestyle changes, diet management, and treatments designed to counteract the effects of hyperglycemia and hyperlipidemia. In virgin and late-pregnant CAF and C rats, we determined body weight, body composition by dual-energy x-ray absorptiometry DEXAglucose tolerance by intravenous glucose tolerance test IVGTTand insulin sensitivity by hyperinsulinemic euglycemic clamp in nonanesthesized rats. Complications linked to diet induced obesity such as impaired glucose utilization and fatty liver can be improved by reducing fat consumption and inducing weight loss. This study did not examine the combined effects of weight loss with exercise but it has been shown that exercise can increase the cutaneous nerve density in diabetic patients without neuropathy and reinnervation capacity in patients with metabolic syndrome [ 3738 ].

Monteiro, P. Table 2 Blood lipids in fasted animals. Interestingly, despite similar intakes and energy expenditure on the LF obrse, a greater rate diet induced obese rat model lipid disappearance was observed in the DR rats compared to DIO rats, suggesting greater basal lipid oxidation in DR rats Coppey, B. Raun K von Voss P Knudsen LB b Liraglutide, a once-daily human glucagon-like peptide-1 analog, minimizes food intake in severely obese minipigs. Increased expression of FGF1-mediated signaling molecules in adipose tissue of obese mice. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publication types

This is likely to result from the additive effects of obesity and pregnancy on insulin sensitivity. Afterwards, rats were transferred to a normal diet or treated with enalapril or dietary enrichment with menhaden oil for 12 weeks. Abstract Objectives: Obesity is one of the most important risk factors for the development of gestational diabetes mellitus GDM.

Animal models of obesity. Finally, platelet signalling studies conducted in PRP and washed platelets are primarily carried out using sodium citrate as anticoagulant. Introduction Obesity is a global public health issue with high prevalence in all age groups [ 12 ]. Dake, and M.

  • Over the years, there have been a number of different modifications to the design of the selection diet that are particularly relevant to note.

  • The motor and sensory nerve conduction velocity was reported in meters per second. Gerbi, J.

  • The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. In an attempt to induce a voluntary hyperphagia, Blancas-Velazquez et al.

  • Table 2 Characterization of the experimental design of the evaluated studies Full size table.

  • Both increased intake and suppressed expenditure led to a large energy imbalance, or energy gap, which resolves gradually as the weight returns Figure 7.

Thus, the aim of the present study was to track the ddiet of obesity and metabolic alterations in the DIO det DR rats fed either a high-fat diet or normal chow diet for 9 months. Interestingly, when compared with sibutramine, the once-daily human GLP-1 analog liraglutide caused model significantly greater weight loss in addition to additional beneficial effects on glucose homeostasis when administered to HE-fed DIO rats for 28 days. In this scenario there is lower production of short-chain fatty acids SCFA, like acetate, propionate and butyrate which leads to less protection of the intestinal epithelium, since SCFA are related to occludin and zonulin, and also leads to a drop in the production of glucagon-like peptide-1 GLP-1 resulting in decreased satiety and increased insulin resistance, inflammation and lipid accumulation [ 24384041 ]. B Platelet isolation protocol was based on a serial of centrifugations. Analysis of platelets from a diet-induced obesity rat model: elucidating platelet dysfunction in obesity. Obesity negativity affects virtually every system of the body and increases the risk for cardiovascular disease, diabetes, osteoarthritis, and many cancers.

Viswanad, L. This suggests that an effective treatment for peripheral neuropathy associated with either prediabetes or diabetes diet induced obese rat model needed and to be efficacious will likely require early detection indjced by a combination of lifestyle changes, diet management, and treatments designed to counteract the effects of hyperglycemia and hyperlipidemia. We previously demonstrated that diet induced obese rats develop whole body insulin resistance and sensory neuropathy associated with reduced sensory nerve conduction velocity, thermal hypoalgesia, and decreased intraepidermal nerve fiber density in the skin of the hindpaw [ 18 ]. Andrade, M.

Journal of Diabetes Research

Qiu, Y. Rinehart et al. Amey Holmes, 1 Lawrence J.

Davidson, 2 and Mark A. Entes et al. Diet induced obese rat model for some of the neural endpoints examined there was a trend toward improvement when diet-induced obese and diabetic rats were placed on a normal diet it is possible that neural function would have improved further if the normal diet was allowed to continue for a longer duration. Maiya, and B. Gispen, L. Effect of reversal of high fat diet, enalapril, or menhaden oil in diet-induced obese or type 2 diabetic rats on nonfasting serum free fatty acids, triglycerides, cholesterol, leptin, and insulin levels. Ansaldi et al.

  • Detailed time-schedule to set up a DIO rat model for platelet studies.

  • Overall, serum leptin levels mirrored the change in the epididymal fat pad weight. Briefly, hind limb sensory nerve conduction velocity was recorded in the digital nerve to the second toe by stimulating with a square-wave pulse of 0.

  • If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To circumvent this limitation, Levin et al.

  • However, this approach is less effective in improving neural deficits. Placing diabetic rats on a normal diet did not improve motor or sensory nerve conduction velocity.

  • Rats fed a high fat diet do not become hyperglycemic, presumably due to compensatory hyperinsulinemia [ 21 ].

  • Skeletal muscle composition in dietary obesity-susceptible and dietary obesity-resistant rats.

Holmes, E. Begg, H. Treating diet induced obese rats or diabetic rats by placing them on the normal diet or to a lesser extent by treating those with enalapril or menhaden oil enriched diet reduced the fatty liver condition. Begg et al.

Following acclimation, rats are provided ad libitum access to the HF diet, which results in a heterogeneous distribution of obsee weight gain in the outbred animals. Mediators Inflamm. Hereditary obesity in the rat associated with hyperlipemia. In terms of energy intake, no differences were found between groups Fig. This inflammatory status can be triggered by a high consumption of saturated fatty acids, which can be found in high concentrations in obesogenic diets [ 27 ]. Mol Nutr Food Res.

Andrade, M. Skip to main content. Moreover, we also measured platelet size by Forward Scatter FSC parameter since it is known to be a common indicator of platelet size.

Giles, E. Related Articles. Hill JO. In order to validate the HE-fed DIO rat as a useful animal model of obesity, we examined the body weight lowering effect of the well-known anti-obesity agent sibutramine and the once-daily human GLP-1 analog liraglutide.

Holmes, B. In diabetic rats, serum free fatty acid, triglyceride, and cholesterol levels were modle significantly increased compared to control rats. View at: Publisher Site Google Scholar. Leptin levels were unchanged in diabetic rats and diabetic rats placed on a normal diet or treated with enalapril or diet enriched with menhaden oil. Figure 1.

  • A Blood collection was done via vena cava with a 19G needle syringe.

  • View at: Google Scholar E. HFSD caused a significant increase in serum triglyceride, low-density lipoprotein cholesterol, and leptin levels and a significant decrease in high-density lipoprotein cholesterol.

  • Also, the obesogenic diet can induce fat ectopic accumulation in the pancreas, which stresses greatly beta cells, disrupting insulin production [ 2327 ]. Drive to regain weight increases with time and is higher early in the relapse period.

  • Academic Editor: Norman Cameron.

  • When taken together, observation of DIO rats in this paradigm of weight regain suggest that adaptive changes in muscle and adipose tissue establish a metabolic context for rapid, energetically efficient weight regain.

Table 3 Changes in markers related to body weight and adipose tissue depots Full size table. Increased visceral fat and decreased energy expenditure during the menopausal transition. Long-term weight-loss maintenance: a meta-analysis of Diet induced obese rat model studies. We observed that prolonged 8-week weight reduction was accompanied by a persistent reduction in TEE that was due in part to a sustained reduction in resting energy expenditure REE. You are using a browser version with limited support for CSS. In subsequent studies, we have observed how regular exercise counters this metabolic drive to regain weight early in relapse; exercise decreases the energy imbalance or energy gap Figure 6 both by reducing appetite and by increasing the level of expended energy during weight regain

Abbott et al. Hereditary obesity in the diet induced obese rat model associated with hyperlipemia. Following acclimation, rats are provided ad libitum access to the HF diet, which results in a heterogeneous distribution of body weight gain in the outbred animals. In Wistar rats the consumption of a high-fat diet appears to lead to an increase in the number of fat cells hyperplasia in the subcutaneous adipose fat, whereas in the visceral adipose fat greater hypertrophy of the adipose tissue is observed [ 60 ].

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Your current browser may not support copying via this button. Tissue oxidative capacity, fuel stores and skeletal muscle fatty acid composition in obesity-prone and obesity-resistant rats. J Clin Endocrinol Metab. Download references. The elevated leptin levels correspond well to the degree of obesity at the time points for the hormone profile.

  • Rather, numerous genes and epigenetic events are involved in generating a polygenic predisposition that favors leanness, obesity, or some level of adiposity between the two extremes, when faced with obesogenic environmental pressures.

  • Dake, and M.

  • Altered sympathetic activity during development of diet-induced obesity in rat.

  • Lijnen HR. Effect of bariatric surgery-induced weight loss on platelet count and mean platelet volume: a month follow-up study.

According to Jirouskova et al. At the time treatments were started there was no statistical difference between the amount of high fat diet consumed by the kodel obese rats and high fat fed rats treated obede a low dose of streptozotocin. While fat droplets were virtually absent in livers from chow-fed animals of either genotype Fig. Obes Rev. Table 1 Inclusion and exclusion criteria used to evaluate the pre-selected articles Full size table. Among the animal obesity models, those that develop a phenotype more similar to human physiopathology are those induced by dietary challenge; in this context, better results are obtained through high-fat diets with high concentrations of saturated fatty acids, since these diets directly affects the metabolism, are palatable and have a high caloric density, which stimulates weight and body fat gain. However, it is frequent to be accompanied by the deposition of lipids ectopic fat in non-adipose tissues, such as the liver [ 5 ].

In the past decades, obesity and associated metabolic complications have reached epidemic proportions. Article dist the Year Award: Outstanding research contributions ofas selected by our Chief Editors. Weight of the left epididymal was significantly increased in diet induced obese rats. Keywords: animal models; diet-induced obesity; high-fat diet; metabolic syndrome; microbiota; obesity. Jung and M. Al-Goblan, M.

Premaratna, E. At this point, animals in the middle group are removed from the study. Fiet, it limits the physical activity of the animals compared to animals housed in a group environment 36as group-housed animals are constantly engaged with one another. Subsequent modifications to the protocol selected the top and bottom tertiles rather than quartiles to represent the extremes of weight gain

Nevertheless, the modulation of the gut microbiota by HF diet was similar in both strains, except for Clostridium leptum that was only reduced in Rat model rats fed with HF diet. Male animals are commonly used in the study of obesity; however, if the study aims to evaluate the brown adipose tissue, females should be used, since this tissue is more easily observed in this sex [ 5051 ]. The authors thank A. Lee, and T. In contrast, leptin levels remained significantly elevated when diet induced obese rats were treated with a diet enriched with menhaden oil. Figure 1.

All diabetic rats were hyperglycemic and this was not affected by treatments. Lessard, J. Efficacy of reversal of the high fat diet obese rat model these endpoints was compared to two distinct treatments that had previously been found to have beneficial effects: angiotensin converting enzyme inhibitor, enalapril, and dietary enrichment with omega-3 n-3 polyunsaturated fatty acids derived from menhaden fish oil a natural source of eicosapentaenoic acid and docosahexaenoic acid [ 1 — 17 ]. Manschot, W. Clinical relevance: The rodent diet-induced obesity model may be useful for unraveling pathomechanisms underlying the association between obesity and periodontal destruction but conclusions have to be drawn with caution. When the diet of rats fed high fat diet for 12 weeks was replaced with a normal diet and analyses performed 12 weeks later, sensory nerve conduction velocity and intraepidermal nerve fiber density were significantly decreased. Motor nerve conduction velocity was calculated by subtracting the distal from the proximal latency measured in milliseconds from the stimulus artifact of the take-off of the evoked potential and the difference was divided into the distance between the 2 stimulating electrodes measured in millimeters using a Vernier caliper.

Introduction

All diabetic rats were hyperglycemic and this was not affected by treatments. Tomaz, P. Davidson, Mark A. The aim of this study was to investigate whether diet-induced obesity results in GDM in rats with the same genetic background.

Zeve, C. When taken together, observation of DIO rats in this paradigm of weight regain suggest that adaptive changes in muscle and adipose tissue establish a metabolic context for rapid, energetically efficient weight regain. Furthermore, the results underscore the effectiveness of GLP-1 mimetics both as anti-diabetes and anti-obesity agents. Holmes, E.

Qiu, Y. Obesity and to a greater extent type 2 diabetes were associated with impaired glucose utilization and peripheral neuropathy. Diabetic rats and diabetic rats placed on the menhaden oil enriched diet weighed about the same as the control rats at the end of the study. Rinehart et al.

The overall previous data in humans are now reinforced by our animal model confirming a hyperactivation of GPVI signalling in obesity. Barrachina, M. Research Diets. Finally, we would like to thank T.

A value of less than 0. Manickam, D. Nassif, J. Lessard, J.

Carreira, B. Tissue oxidative capacity, fuel stores and skeletal muscle fatty acid composition in obesity-prone and obesity-resistant rats. No use, distribution or reproduction is permitted which does not comply with these terms. Google Scholar.

Journal of Diabetes Research

Davidson, B. Yorek, L. The mean of the measurements reported in sec were used as the thermal nociceptive response. Davidson, and M. Lamping, D.

Motor and Sensory Nerve Conduction Velocity On the day of terminal induuced rats were weighed and anesthetized with Nembutal i. Louis, MO. Al-Goblan, M. Diet induced obese rats weighed significantly more than control rats after 24 weeks on the high fat diet. Crugeiras, M. As previously reported, treating type 2 diabetic rats with a high fat diet containing enalapril and to a greater extent with a high fat diet enriched with menhaden oil slowed the progression or improved diabetic neuropathy endpoints [ 130 ].

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Shevalye, M. Immunoreactive intraepidermal nerve fiber profiles, which are primarily sensory nerves, were visualized using confocal microscopy. Placing diet induced obese rats on a rat model diet or treating them with enalapril but not menhaden oil corrected the left epididymal fat pad weight toward control levels. Effect of reversal of high fat diet, enalapril, or menhaden oil in diet-induced obese or type 2 diabetic rats on motor and sensory nerve conduction velocity, thermal nociception, and intraepidermal nerve fiber density. Reed, K. Academic Editor: Norman Cameron.

View Table. The OR rats, however, appear to sense the nutrient overload and adjust their food intake and increase their energy expenditure to reestablish energy balance. Figure 5. View all 17 Articles.

Liu, Y. Placing diabetic rats on a normal diet or infuced them with enalapril or diet induced obese rat model oil enriched diet lowered serum lipid levels compared to untreated diabetic rats. In obese patients with type 2 diabetes a year after having undergone gastric bypass surgery there was a significant improvement in weight, blood glucose, hemoglobin A 1 C, and insulin resistance and the percentage of patients with neuropathy was lower than the number of cases at baseline [ 34 ]. Oltman, and M. Kaul, and P.

Manickam, D. Legrand-Poels, J. Publication types Research Support, Non-U. Nassif, J.

However, the susceptibility to obese rat in response to this challenge is highly dependent upon the strain of the animal 11 — Src family kinases: at the forefront of platelet activation. Leite, N. We want to highlight that the aim of this study was to evaluate the induction of obesity through the diet. These observations suggest that the impact of OVX on energy balance and fuel utilization is different for DIO and DR rats in this paradigm and that this difference may affect the latency, survival, and growth of mammary tumors. However, no differences were found on platelet size among groups. Fully-automated, high-throughput micro-computed tomography analysis of body composition enables therapeutic efficacy monitoring in preclinical models.

Motor and sensory nerve conduction velocity was partially improved by treating diabetic rats with enalapril and to a greater extent by treating diabetic rats with a diet enriched with menhaden oil. Begg et al. Crugeiras, M. Liu, Y. Papanas, A.

A value of less than 0. Skip to main content. Obesity-prone OP rats were maintained on a HF diet for rxt weeks to induce obesity. This approach can be applied to test weight reduction strategies for their ability to overcome the metabolic pressures driving weight regain by modifying the environmental conditions in the treatment phase and examining the response during the relapse phase. Coppey, Eric P.

Thermal latency was increased but was not significantly different from either control or rats fed a high fat diet for 24 weeks. Entes et al. Louis, MO. Complications linked to diet induced obesity such as impaired glucose utilization and fatty liver can be improved by reducing fat consumption and inducing weight loss.

Non-fasting HE-fed DIO rats had elevated basal levels of leptin and insulin throughout the h period of measurement at 3, 6, and 9 months of age Fig. Obesity 26— Coppey, A. It should be noted that we did not measure pancreatic function directly in the present study, and therefore cannot exclude that the observation should be ascribed to a difference in the level of insulin clearance. The animals were defending a target weight that was drifting upwards while they were weight reduced, an effect we attribute to age. Behavioral responses to orexin, orexin receptor gene expression, and spontaneous physical activity contribute to individual sensitivity to obesity.

Al-Alfi, and M. Amil, and F. Matsuda and I. The present investigation was to evaluate a common rat model, in which obesity is induced by high-fat, high-sucrose diet HFSDfor its applicability in periodontal research.

Maiya, and B. The two rat models used in these studies were the diet induced obese and type 2 diabetic rat models. Intraepidermal Nerve Fiber Density in the Hindpaw Immunoreactive intraepidermal nerve fiber profiles, which are primarily sensory nerves, were visualized using confocal microscopy.

Vague, G. Nonfasting blood glucose was determined. In contrast, treating diet induced diet induced obese rat model rats rst enalapril and to a greater extent with a diet enriched with menhaden oil improved sensory nerve conduction velocity. Figure 1. Placing diet induced obese rats on a normal diet did not improve sensory nerve conduction velocity. The remaining group was maintained on a normal diet Harlan Teklad,3.

Oobese diet induced obese rats on a normal diet or treating them with enalapril lowered serum leptin levels. Maixent, J. Foreyt and W. Placing diet induced obese rats on a normal diet did not improve sensory nerve conduction velocity. This was expected since leptin is mainly produced by adipose tissue and its circulating levels correlate with the amount of body fat [ 33 ].

Liu, Y. Stanley, D. We previously demonstrated that diet induced obese rats develop whole body insulin resistance and sensory neuropathy associated with reduced sensory nerve conduction velocity, thermal hypoalgesia, and decreased intraepidermal nerve fiber density in the skin of the hindpaw [ 18 ].

Immunoreactive intraepidermal nerve fiber profiles, which are primarily sensory nerves, were visualized using confocal microscopy. Henriksen and M. S5—S11, Meszaros, L. Liu et al.

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These differences in food intake suggest that there are preexisting differences in regions of the brain that regulate diet induced obese rat model behavior. Malik, S. Obesee View author publications. Increased levels of platelet adhesion to collagen-coated plates were observed in the obese group Fig. In two subsequent studies with females 3940we adjusted our approach and ranked animals by their rate of weight gain in the obesogenic environment from 10 to 18 weeks of age.

The gut microbiota of SD rats was less abundant in Bacteroides and Prevotella but richer in Bifidobacterium and Lactobacillus comparatively to the gut microbiota of Wistar rats. Coppey, B. Ansaldi et al. Rats were briefly anesthetized with isoflurane and the glucose solution was injected.

Data in Table 1 demonstrate that the beginning weight of all the rats in the study were statistically the same. To assess some of the features of the metabolic syndrome, oral glucose tolerance tests, systolic blood pressure measurements and blood biochemical analysis were performed throughout the study. Kaul, and P.

Dift, and F. Kappelle, and G. We previously characterized the progression of neuropathic deficits in this model that included severe insulin resistance compared to diet induced obesity rats and a decrease in motor and sensory nerve conduction velocity as well as deficits associated with thermal nociception [ 19 — 21 ]. This was expected since leptin is mainly produced by adipose tissue and its circulating levels correlate with the amount of body fat [ 33 ].

Tomaz, P. Davidson, L. Sensory nerve conduction velocity was determined using the digital nerve as described [ 121 ]. Davidson, and M. Davidson, B. In the past decades, obesity and associated metabolic complications have reached epidemic proportions.

During a similar time period, Levin published similar findings using a different strain and a different obesity-inducing diet. Counterstaining was performed diet induced obese rat model Gill's hematoxylin solution. Treating diet induced obese rats or diabetic rats by placing them on the normal diet or to a lesser extent by treating those with enalapril or menhaden oil enriched diet reduced the fatty liver condition. Obesity is one of the main health problems in industrialized countries. Western blotting was performed to analyze individual samples biological replicates for validation purposes.

Although riet HE-fed DIO rat never develops frank diabetes, diet induced obese rat model day chronic dosing study with sibutramine and the novel GLP-1 analog liraglutide demonstrates the versatility of the HE-fed DIO rat as a polygenetic model of human obesity and the associated metabolic alterations. Manickam, D. Trafficking of dietary fat in obesity-prone and obesity-resistant rats. Enhanced metabolic efficiency persisted throughout this early period of relapse and contributed to the suppressed TEE. After reading the selected articles, one additional article was included in the study, totaling 35 articles Fig.

  • Src family kinases: at the forefront of platelet activation. Am J Physiol 3 Pt 2 :R—

  • Jackson, and A.

  • Diabetol Metab Syndr 13, 32 Placing diet induced obese rats on a normal diet or treating them with enalapril lowered serum leptin levels.

Weisinger, K. The diabetes in invuced rats is analogous to the development of human type 2 diabetes when the decline in hyperinsulinemia is not able to compensate for insulin resistance and results in the development of hyperglycemia [ 19 ]. Placing diet induced obese rats on a normal diet did not significantly improve intraepidermal nerve fiber density. Premaratna, E. It has been shown that humans and animal models of prediabetes and insulin resistance have sensory neuropathy like deficits [ 12126 — 29 ]. Vague, G. Results from dietary correction were compared to the effect of treatment with enalapril or enrichment of the diet with menhaden oil.

In summary, the present study allowed to establish an adequate blood collection and platelet isolation method for DIO rats and contributes to elucidate platelet dysfunction in obesity. The experiment was preceded by a 3-day run-in period with mock gavages. J Physiol Bochem. Am J Clin Nutr 70 4 —3. New insights into the role of adipose tissue in thrombosis. In our case, we found that platelet counts were significantly higher in the DIO model compared to control rats. This occurred at an average of

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