Turkey, stuffing, mashed potatoes, and gravy - cranberry sauce, pumpkin pie, and dinner rolls - these are the traditional foods of Thanksgiving.
Here’s a little secret, though: the familiar flavors of your Thanksgiving favorites can be had without piling on the carbs. To study the pathogenesis of diabetic cardiomyopathy, reliable animal models of type 2 diabetes are required.
High-fat feeding in combination with a low dose of STZ induced cardiac metabolic changes that mirror the decrease in glucose metabolism and increase in fat metabolism in diabetic patients.
IntroductionThe incidence of type 2 diabetes continues to increase, despite the best current therapies and educational programs available. Hepatic intracellular substrate storesHepatic triglyceride and glycogen stores were measured as an indicator of changes in liver metabolism. Hepatic triglyceride and glycogen concentrations in control and diabetic rats following high-fat feeding in combination with low dose STZ. Cardiac intracellular substrate storesOne of the main aims of this study was to characterise the cardiac metabolic phenotype of this new model of type 2 diabetes.
Cardiac triglyceride and glycogen concentrations in control and diabetic rats following high-fat feeding in combination with low dose STZ. Cardiac pyruvate dehydrogenase, medium chain acyl-coenzyme A dehydrogenase (MCAD) and citrate synthase activities in control and diabetic rats following high-fat feeding in combination with low dose STZ. Cardiac metabolic proteinsAs the changes in metabolic enzymes displayed dose-dependent relationships between STZ dose and activities, we, therefore, investigated which doses of STZ induced changes in metabolic protein expression.
Cardiac pyruvate dehydrogenase kinase 4 (PDK4), glucose transporters (GLUT) 4 and 1 protein levels in control and diabetic rats following high-fat feeding in combination with low dose STZ. DiscussionThis study has demonstrated that high-fat feeding in combination with a low dose of STZ is sufficient to induce the cardiac metabolic phenotype present in type 2 diabetes.
AcknowledgementsWe thank Emma Carter and Lydia Le Page for technical assistance, and Rhys Evans for constructive discussion of the data.
Competing interestsThe authors declare that they have no competing interests.Authorsa€™ contributionsLM conducted the isolated heart perfusion experiments, enzyme assays and tissue analysis. Although keeping a properly balanced diet and eating healthy is often puzzling, you can gain success. We will give you some excellent tips to attain you in achieving success in your weight loss.
This means you don’t need to worry about lowering of metabolism as well as about any other health issues. Breakfast (Spinach and cheese omelette): one cup spinach, one ounce Swiss cheese, 2 large eggs, one muffin, one orange. Lunch(Honey mustard chicken pita with cucumber salad): 3 oz grilled sliced chicken, one whole grain pita, ? cup baby spinach, ? cups sliced cucumber, 2 tbsp. Dinner: South Pacific Shrimp, Warm beet and spinach salad, ? cup cooked couscous, one whole wheat roll, 1 medium peach. Dinner: chicken breasts with mushroom sauce, one cup cooked brown rice, ? cup steamed asparagus, broiled mango.
1800 ADA (American Diabetic Association) diet menu plan recommends an effective and healthy diet that is balanced in calories, dense in nutrients and low in fat and sodium. Due to ADA recommendations, carbohydrate servings should be evenly distributed throughout the day.
Lunch: Ham and veggie pita (? wheat pita, 3 ounce turkey ham, 5 sliced cherry tomatoes, 1 tbsp.
If you are diabetic, you need to avoid such foods as: candies, cookie, cake, granola bars, ice creams, pastries, jelly and jam, sugar covered cereals, sodas, colas, sweet rolls, etc.
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The low-carb Paleolithic diet is more effective for producing weight loss, melting belly fat, and controlling diabetes than a low-fat diet, according to research conducted by scientists at Umea University in Sweden and published in the European Journal of Clinical Nutrition. The two-year study tracked 70 overweight, post-menopausal women who were assigned either a low-fat diet or a low-carb (higher-fat) Paleo diet.
Study participants were measured for weight, cholesterol and blood sugars after six months on their respective diets, and again after two years.
What's more, the low-carb, high-fat Paleo dieters lost 4 inches from their waists after six months, compared to just 2 inches for the low-fat dieters.
The results are noteworthy because older women — especially those who are post-menopausal — have historically reported having a hard time losing weight, especially from their mid-sections, due to slower metabolisms and hormone disruptions. Researchers said Paleo dieters also reported feeling more satisfied and less hungry than low-fat dieters, which makes sense, since fat makes food taste better and boosts satiety. The Paleo diet emphasizes high-quality animal proteins, healthy fats, vegetables and fruits, and excludes gluten, sugar, dairy, legumes, starches, alcohol and processed foods. Two excellent resources on the Paleo diet are The Paleo Solution (by Robb Wolf) and The Primal Blueprint by Mark Sisson, who is his own best advertisement for the anti-aging benefits of the Paleo eating plan.
The new Swedish study bolsters claims by leading obesity experts who insist low-carb diets like the Paleo and ketogenic diets fuel rapid weight loss, reverse type 2 diabetes, and prevent Alzheimer's, obesity, epilepsy and ADHD.
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Express delivery arrives 1-2 days after dispatch or for heavy parcels Courier 1-2 days after dispatch Mon-Thu. Physiologically relevant rodent models are needed, which not only replicate the human pathology but also mimic the disease process.
Cardiovascular disease is the leading cause of mortality in type 2 diabetic patients in the United Kingdom [1]. All procedures were in accordance with Home Office (UK) guidelines under The Animals (Scientific Procedures) Act, 1986 and with institutional guidelines.


Three weeks of high-fat diet alone did not change hepatic triglyceride or glycogen concentrations compared with controls (Figure 1). Cardiac triglyceride concentrations were increased by all doses of STZ tested, compared with control rats, but not by high-fat diet alone, displaying a significant positive correlation with STZ dose (Figure 2).
Proteins involved in cardiac glucose metabolism were investigated in our model of type 2 diabetes, to determine if this pathway was downregulated in diabetic hearts (Figure 4).
In general, this model displayed hyperglycaemia, normoinsulinaemia and hepatic lipid deposition. Rats were fed a chow or high-fat diet for 21 days, with STZ injected at varying doses at day 14.
The main problem is that we often don’t know what portions and serving sizes of food are allowed. 1800 caloric range offers a wide variety of healthy food safe and easy to carry out on you own. Get yourself through the week with our healthy 1800 calorie meal plans without ruining your diet. Consistent eating throughout the day will help you to improve diabetes medications’ efficacy.
However, whether you are aiming at losing your weight or controlling diabetes, correct meal planning is a solution. The results showed the Paleo dieters lost significantly more weight (14 pounds) compared to the low-fat dieters (5.7 pounds). In previous studies, the Paleo diet has routinely beaten low fat diets at controlling cholesterol and diabetes. It's the most popular diet around today, and has a large celebrity following, including NBA superstars Kobe Bryant, Blake Griffin and Ray Allen, supermodel Adriana Lima (pictured above), and actor Kellan Lutz. David Perlmutter told me the Paleo diet can curb today's alarming epidemics of degenerative disease, including dementia.
Thanksgiving might be a feast day in which we give thanks, but for those whose health dictates a low-carb diet, Thanksgiving might seem like nothing but a plate of turkey.
Here we characterised cardiac metabolic abnormalities, and investigated the optimal experimental approach for inducing disease, in a new model of type 2 diabetes. Metabolic changes in the heart have been implicated in the increased incidence of myocardial infarction [2], with diabetic patients having decreased cardiac glucose metabolism and increased cardiac fatty acid metabolism [3a€“6]. Combining high-fat diet with all doses of STZ tested increased hepatic triglyceride concentrations, compared with control rat livers. Protein levels of the PDH inhibitor pyruvate dehydrogenase kinase 4 (PDK4), were increased by all doses of STZ compared with controls.
Diabetic hearts had decreased proteins involved in glucose metabolism with a concomitant increase in proteins involved in fat metabolism. MC, DT, CC and KC conducted the animal experiments, assisted with data analysis and helped to draft the manuscript. Carbs, proteins, fats and calories are balanced providing optimum nutrition to the patients with diabetes.
With correct diet meal plans controlling blood glucose levels and losing your weight can be easy and enjoyable. There was a dose-dependent increase in blood glucose and plasma lipids with increasing concentrations of STZ. Therefore, a greater understanding of how type 2 diabetes affects the heart, the role of abnormal cardiac metabolism and how novel interventions could circumvent this are needed.Animal models of type 2 diabetes are currently the first line for investigating disease mechanisms and pharmacological therapies. These changes in PDH and MCAD activity were independent of a change in the Krebs cycle enzyme citrate synthase, used as a marker of overall mitochondrial content. In contrast, the insulin-responsive glucose transporter, GLUT4, protein levels decreased with all doses of STZ, compared with control hearts. Thus, even at the lowest dose of STZ, glycolytic rates were suppressed in the hearts of these type 2 diabetic rats. Many metabolic parameters displayed a dose-dependent relationship with STZ, with the highest dose of STZ inducing a metabolic profile that more closely resembled type 1 diabetes. Cardiac and hepatic triglycerides were increased by all doses of STZ, in contrast, cardiac glycogen concentrations increased in a dose-dependent manner with increasing STZ concentrations.
For relevance to humans, animal models must replicate the phenotype seen in patients as closely as possible, but it is also desirable that they mimic the developmental process of the disease. Epididymal fat pad weight, an indicator of total body adiposity, and fat pad to body weight ratio were significantly increased with higher doses of STZ compared with controls. Cardiac glucose transporter 4 protein levels were decreased, whereas fatty acid metabolism-regulated proteins, including uncoupling protein 3 and pyruvate dehydrogenase (PDH) kinase 4, were increased with increasing doses of STZ. From a practical perspective, models that are easy to generate, cheap and develop in a timely manner will be favoured over expensive and time-consuming models.
On day 13, rats were fasted overnight and given a single intraperitoneal injection of streptozotocin (STZ in citrate buffer, pH 4) the following morning, and the high-fat diet feeding was continued for a further week (or chow diet for controls).
Only this high dose of STZ induced weight loss, and produced a plasma metabolite profile that included hyperketonaemia, hyperlipidaemia, and hypoinsulinaemia.
Cardiac PDH activity displayed a dose-dependent relationship between enzyme activity and STZ concentration.
No animal models are perfect, and current rodent models of type 2 diabetes have been associated with a number of drawbacks (comprehensively reviewed by Bugger and Abel [7]). NEFA non-esterified fatty acids, I?-OHB I?-hydroxybutyrate, control na€‰=a€‰11, for diabetic groups na€‰=a€‰4. Markers of cardiac fatty acid metabolism were also assessed, to determine if this pathway was upregulated in our diabetic hearts (Figure 5). This is in agreement with other studies that have used high doses of STZ in isolation or in combination with high-fat feeding [19, 36a€“39], with these high doses also causing abnormalities in liver morphology and function [25].
In contrast, the lower doses of STZ investigated in the present study avoided these extreme phenotypes, instead presenting with hyperglycaemia in the absence of ketosis, normoinsulinaemia and with maintenance of body weight.
Similarly, the Goto-Kakizaki GK rat is insulin resistant but remains lean [12, 13], making comparisons to the human condition and its association with obesity difficult.


After three weeks on their designated diet, rats in the fed state were terminally anaesthetised with sodium pentobarbital, hearts and livers were rapidly excised, freeze clamped and stored at a?’80A°C for subsequent analysis. Another drawback of spontaneously diabetic and transgenic animals is the expensive cost of purchase [14]. Following excision of the heart, blood was collected from the chest cavity, plasma separated and analysed for metabolites using a Pentra analyser (ABX, UK) and an insulin ELISA (Mercodia, Sweden).
MCT1, responsible for ketone body and monocarboxylic acid uptake, was measured, to determine if changes in this transporter mirrored changes in plasma ketone bodies. In relation to cardiac research, one of the limitations of current rat models is the extended periods taken to develop cardiac phenotypes, despite the presence of abnormal circulating metabolites from an early age. Both left and right epididymal fat pads were excised, trimmed and weighed, for assessment of adiposity.Tissue analysisCardiac and hepatic glycogen content were determined by the breakdown of glycogen to glucose units, using amyloglucosidase.
There were no significant differences between groups in cardiac MCT1 protein levels, although there was a general trend for lower levels in diabetic hearts compared with control hearts. This metabolic shift has been demonstrated in a number of animal models of diabetic cardiomyopathy [44, 45], and has been implicated in the increased incidence of, and decreased recovery following, myocardial infarction [2]. Triglyceride content was measured in cardiac and hepatic tissue, following Folch extraction, using a kit from Randox, UK.
In our diabetic hearts, we found markers of fatty acid oxidation, such as UCP3, were upregulated. The active fraction of pyruvate dehydrogenase was assayed in cardiac homogenates according to the protocol of Seymour et al.[28].
UCP3, MCAD and PDK4 are peroxisome proliferator-activated receptor I± (PPARI±) targets, a transcription factor that is activated by fatty acid ligands to upregulate fat metabolism, and is increased in diabetes [46]. STZ is traditionally used at high doses to induce type 1 diabetes, as it results in impaired insulin secretion from the I?-cell [20, 21].
Medium chain acyl-coenzyme A dehydrogenase activity in cardiac homogenates was measured by following the decrease in ferricinium ion absorbance, as described by Lehman et al.[29]. The activation of PPARI± in diabetes is due to both the increased intake of dietary fatty acids, in addition to increased adipose lipolysis associated with adipose insulin resistance [47].
In contrast to fatty acid metabolism, proteins involved in cardiac glucose metabolism, such as GLUT4, were downregulated in our diabetic hearts. This would mimic the human disease process resulting in a metabolic phenotype similar to that in late stage type 2 diabetic patients. Thus, the changes in protein and enzyme activity in our diabetic hearts would fully support the shift away from glucose metabolism towards fat metabolism, reported in other models and in patient studies [48].
This model has become increasingly popular in recent years, both for investigating the mechanisms involved in type 2 diabetes and for testing potential therapies [22a€“26].
Future studies to measure the effects on fatty acid and oxidative metabolism in this model will confirm the link between the changes in mitochondrial proteins and flux through these pathways.Perfused heart studies allow the simultaneous measurement of metabolic flux and contractile function in the isolated organ. However, the degree of diabetes induced, the amount of STZ used, background strain and starting body weight vary considerably between these studies. The decrease in glycolysis was independent of impaired cardiac systolic function or loss of mitochondria, suggesting that the glycolytic changes were not secondary to adverse cardiac remodelling and mitophagy.
Antibodies against GLUT1 and UCP3 were purchased from Abcam, UK, and against monocarboxylate transporter (MCT) 1 from Santa Cruz. In a clever study by Marsh et al., the interaction between diet and diabetes on cardiovascular function was investigated, using a similar model to our current study [51].
They demonstrated that a combination of high-fat feeding and low dose STZ increased diastolic wall stress and arterial stiffness, as occurs in patients with type 2 diabetes, but that modifying only diet or using only STZ did not produce this effect, despite increased blood glucose and abnormal insulin tolerance tests, respectively [51]. The advantages of this model are that the disease is induced over a relatively short time and without high costs.
In addition, we aimed to determine the optimal experimental approach to induce the disease by testing the cardiac effects of a variety of STZ doses in mature adult Wistar rats.
Left ventricular developed pressure was determined as systolic pressure minus end-diastolic pressure.
In addition, the dose of STZ can be manipulated to match the degree of diabetes required for the study. Our results showed that inducing type 2 diabetes, using a combination of high-fat feeding with a low dose of STZ, mimics the human condition. Similarly, in a study by Islam and Choi, the high-fat diet in combination with low dose STZ model was identified as a better model of type 2 diabetes than an alternative chemically-induced model that utilised an injection of nicotinamide prior to administration of STZ [37].
We found it was essential to fast the rats prior to STZ injection, as preliminary experiments demonstrated a much lower success rate for inducing diabetes if injections were carried out in the fed state (data not shown). This is likely related to the mode of action of STZ, a glucosamine-nitrosourea antibiotic that competes with blood glucose for the pancreatic I?-cell GLUT2 receptor [20].Hepatic and cardiac triglyceride concentrations were elevated by all doses of STZ tested but not by high-fat diet alone, indicating that this was due to the combination of STZ and high-fat. To investigate the STZ dose-dependent effects, a two tailed regression analysis was performed between the five doses of STZ. Hepatic and cardiac glycogen concentrations showed dose-dependent relationships with STZ concentrations, but in opposite directions in the two organs; decreasing in liver but increasing in heart. However, at no time did we see an increase in fed insulin concentrations, which has been observed in a number of other models. It has been suggested that this is due to STZ causing a small degree of I?-cell damage, which is sufficient to limit the upregulation of insulin secretion in response to the systemic insulin resistance [19]. Using a glucose tolerance test, they demonstrated systemic insulin resistance with high-fat diet alone [19]. This model also has the added advantages of being relatively inexpensive, easy to induce and can be modified for different severities of diabetes, according to requirement of the study.



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