All values in the table represent the percentage of the total dry weight of the diet for the indicated carbohydrate or fatty acid.
Weight gain and basal blood glucose and insulin, (A) Bodyweight was measured once weekly for the 8 week study period. Intravenous glucose tolerance tests were performed after 8 weeks of feeding with the respective diets. A most critical property of any diet induced obesity model used to study T2D, is the induction of insulin resistance by the diet. Not only will I embed the videos onto this page, I will also include the most important information you should learn from each video. After you have gone through the videos, go through theĀ Pediatric Advanced Life Support (PALS) Provider Handbook by Dr. The book covers the important things, without bogging you down with low-yield, nitpicking details. Different high fat diets are used and in order to determine which diet produces a model most accurately resembling human T2D, they need to be compared head-to-head.
IntroductionObesity and diseases associated with it, represent a rapidly growing health problem in both developed and developing countries [1]. The values for the fat source represent the percentage of the total kcal from fat derived from the indicated source. Intravenous Glucose Tolerance TestsAn Intravenous glucose tolerance test (IVGTT) was performed on 5-h fasted mice after 8 weeks of diet treatment. Plasma glucose was significantly elevated during the 75 min IVGTT in the high fat diet group compared to the normal diet control, whereas there were no significant differences in plasma glucose levels between the high fat-high sucrose diet and the high sucrose control diet groups (Figure 2A,B). Linear regressions between the glucose elimination rate (KG) and the acute insulin response (?AIR) for the normal and high fat diet groups (A) and the Surwit high sucrose and high-fat high sucrose diet groups (B).
We evaluated this by the euglycemic-hyperinsulinemic clamp, which is the most accurate method for determining insulin sensitivity.
Glucose tolerance, as assessed by the glucose elimination constant KG, was however significantly impaired in both high fat diet groups compared to their respective controls (Figure 2C). Mice that had been fed one of each of the experimental diets were subjected to euglycemic-hyperinsulinemic clamp studies.
Results: Mice fed a HFD gained more weight than HFHS fed mice despite having similar energy intake. There are clear biochemical relations between obesity and T2D, where changes in obesity predispose susceptible individuals to develop T2D. Since I like to march to the beat of my own drum, I opted to find my own … on the cheap!
And by the end, you will not only memorize the high-yield information ā€¦ you will also understand it.
An important mechanism is that the expansion of adipose tissue depots that occurs in obesity leads to elevated levels of adipocyte-derived hormones, circulating free fatty acids and pro-inflammatory cytokines.

The incremental area under the curve (AUC) for insulin was similar between the normal and high fat diet groups, whereas there was a 2.7 fold increase in AUC in the high fat-high sucrose group compared to the high sucrose control diet group (Figure 2E). The glucose infusion rate for the high fat diet group was 80% lower than that of the normal diet group (Figure 4C). Spend just a little effort follow my instructions and you should have no problem getting certified, even if you never seen the materials before in your life.
Some of these factors contribute to peripheral insulin resistance in the liver, adipose tissue and skeletal muscle [3]. Blood samples were taken from the retrobulbar intraorbital plexus after a 5 h fast and plasma was assayed for glucose (B) and insulin (C).
The acute insulin response (AIR) to the glucose challenge was not different between the normal diet and the high fat diet groups, but it was significantly higher in the high fat-high sucrose group than in the high sucrose control diet group (Figure 2F). The glucose infusion rate in the high fat-high sucrose diet group however, was only 37% lower than that of the high sucrose control diet group (Figure 4C). The acute insulin response (AIR) was unchanged in the HFD group, but slightly increased in the HFHS diet group. The insulin resistance in turn would cause impaired glucose tolerance, however most individuals are able to adapt to the insulin resistance through a compensatory increase in insulin secretion resulting in normal circulating glucose levels.
The HFHS diet group had a threefold greater total insulin secretion during the IVGTT compared to its control, while no differences were seen in the HFD group.
Adaptation to the insulin resistance by increasing insulin secretion reaches a critical point in some individuals where they can no longer maintain insulin secretion at such high levels [4]. In the normal diet group the rate of glucose elimination (KG) positively correlated with the acute insulin response (Figure 3A). Insulin sensitivity was decreased fourfold in the HFD group, but not in the HFHS diet group. Pancreatic beta cell function becomes at this point insufficient resulting in fasting and postprandial hyperglycemia and eventually type 2 diabetes.
Conclusion: The HFD and HFHS diet models show differential effects on the development of insulin resistance and beta cell adaptation. It is known that reduced beta cell volume and function are associated with the insulin insufficiency seen in impaired glucose tolerance and T2D [4,5]. Surprisingly, there was no relationship at all between KG and the acute insulin response in either of the high sucrose diet groups (Figure 3B). The blood insulin level at the end of the 90 min euglycemic-hyperinsulinemic clamp (clamp insulin) was significantly elevated for the HFD group compared to all other groups (Figure 5B).
These discrepancies are important to acknowledge in order to select the appropriate diet for specific studies.
With the reduced beta cell volume and function, the counter-regulation of glucagon secretion is lost resulting in fasting and postprandial hyperglucagonemia which contributes to the existing hyperglycemia [6]. As islet adaptation to insulin resistance is critical to preventing the onset of T2D, treatment strategies that involve restoring or maintaining beta cell function are currently in use and new treatments are actively being pursued.In the development of new treatments for T2D the necessity for reliable animal models is of the utmost importance.

However after several weeks, high fat fed mice show increases in their acute insulin response to a glucose challenge and improved glucose disposal resulting in a near normalization of glucose tolerance [9]. The increased beta cell mass and insulin secretion result in higher fasting and postprandial insulin levels and normalized glycemia [10,11].
There are however key differences that limit the high fat diet fed mouse model in the study of diabetes. The acute insulin response (AIR) was calculated as the mean of the suprabasal 1 and 5 min values, while ?AIR was calculated as the mean of the suprabasal 1 min value only. The glucose elimination constant (KG) was calculated as the slope of the logarithmically transformed circulating glucose concentration between 5 and 20 min after administration of the glucose bolus. In human obesity, more modest increases in beta cell volume from 20% to 50% have been reported [13,14]. Some obese insulin resistant humans will experience beta cell failure and insulin levels will no longer be sufficient to maintain normal glycemia. Once this process begins, fasting and post-prandial hyperglycemia and eventually overt diabetes is the result. In both cases the energy intake was the total energy intake for each cage of mice and weight gain was determined as the sum of the weight gained by all the mice in a given cage. Mice fed a high fat diet do not develop the progressive beta cell failure seen in human diabetes [8], so diet induced obesity mouse models do not develop overt T2D as is the case in the human disease.
Comparisons between the experimental and control groups were performed by the Mann-Whitney U-test. Metabolic studies performed in rodents from different research labs have yielded some variable results.
There are many reasons why this may be the case, such as gender, age, mouse substrain, use of anesthetics among others.
Whether or not the different high fat diets used to induce obesity and insulin resistance in mice contributes to this variation may also be discussed. Other diets which are proposed to more closely mimic human diets have been described [15,16,17].
Although all of the diets are reported to induce obesity, the amount and source (animal or vegetable) of fat and the composition of other macronutrients are different in different diets.
In order to determine which dietary regime results in the most appropriate mouse model for studies on obesity, glucose intolerance and islet adaptation to insulin resistance, the diets need to be evaluated in head to head comparisons. This study describes a head to head comparison of the two most commonly utilized diet induced obesity models for the study of obesity and type 2 diabetes, with a focus on the increased insulin secretion in response to insulin resistance as the primary endpoint.

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