Scientists are interested in determining the underlying metabolic reprogramming events that lead to type 2 diabetes mellitus (T2DM), a disease characterized by insulin resistance and increased hepatic glucose production.  MicroRNAs (miRNAs) are a class of small noncoding RNAs implicated in T2DM pathology.  miR-26a, a member of the miR-26 family of miRNAs, has been shown to play a critical role in regulating hepatic glucose production and lipid metabolism.  miR-26a has also been implicated in the prevention of obesity-induced insulin resistance, as evidenced by decreased miR-26a expression in obese, leptin-deficient (ob/ob) mice compared to lean control mice.Experiment 1Researchers designed an experiment to promote obesity-induced insulin resistance in wild-type (WT) mice and Alb Tg mice, which express hepatic miR-26a at levels three-fold greater than WT.  WT mice and Alb Tg mice were fed either a standard healthy diet (SHD) or a high-fat diet (HFD) for 14 weeks.  All mice were then fasted for 13 hours and received an abdominal injection of a glucose preparation (2 g/kg of body weight).  The mice were then fasted for 10 hours to allow blood glucose levels to return to baseline, after which an insulin preparation (1 U/kg of body weight) was injected in the abdomen.  Blood samples were drawn from the tail veins of all specimens to assess serum glucose levels.  Figure 1 shows the experimental results for WT mice and Alb Tg mice fed a HFD.Figure 1  Effect of glucose and insulin administration on blood glucose of WT and Alb Tg mice fed a HFD.  (Note:  WT and Alb Tg mice fed a HFD had equal weight gain.)Experiment 2Blood samples were taken from fasting human adults, and levels of hepatic miR-26a were measured in comparison to a ubiquitously expressed reference gene, RNU24.  Figure 2 shows the miR-26a levels plotted against each subject's body mass index (BMI, the ratio of body mass to squared body height).Figure 2  Relationship between BMI and hepatic miR-26a expressionAdapted from Fu, X., Dong, B., Tian, Y., Lefebvre, P., Meng, Z., Wang, X., Pattou, F., Han, W., Wang, X., Lou, F., Jove, R., Staels, B., Moore, D.D., & Huang, W. (2015). MicroRNA-26a regulates insulin sensitivity and metabolism of glucose and lipids. The Journal of Clinical Investigation, 125(6), 2497–2509. Question 59One of the human study subjects with a BMI of 56 kg/m2 (Figure 2) is discovered to have a pathology similar to ob/ob mice.  Like ob/ob mice, individuals affected by this pathology exhibit normal weight at birth but become severely obese afterward and have undetectable levels of leptin in the serum.  What is the best explanation for the absence of serum leptin in this subject?A.Leptin cannot bind its receptor in the hypothalamus.B.Leptin cannot bind its receptor in the thyroid gland.C.Leptin cannot be secreted from gastric cells.D.Leptin cannot be secreted from adipocytes.

hich of the following will give well annotated metabolic pathway miRbase blastdb KEGG Ensembl

Colon cancer is one of the major killers in Western societies. Scientists are continually trying to develop new methods for early detection and diagnosis of this disease. It’s been recognized that cancer cells in part start to proliferate due to the failure to regulate the transcription of certain types of RNA, known as microRNAs. Therefore researchers are trying to identify if there are certain microRNAs which can be used as diagnostic markers of colon cancer. Wu et al. (2015) analysed one such microRNA (miR-1) and carried out screening from 56 subjects (28 healthy, 28 with colon cancer) to evaluate counts of miR-1 transcripts in the colonic mucosa. They predicted that levels of miR-1 would be much higher in cancer patients. The data are in the file sle251coloncancer. In this file the column 'tissue type' is the type of tissue sampled in regard to whether it was taken from a sick (cancer) patient or a healthy (normal) patient. The column 'count' is the number of miR-1 fragments detected in that particular individual (per 100 microlitres). Question 1 (1 point) What is the null hypothesis tested in this study? Question 1 options: The mean amount of miR-1 is greater in healthy patients compared to cancer patients. The mean amount of miR-1 is smaller in healthy patients compared to cancer patients. There is no difference in the standard error of miR-1 amount between cancer patients and healthy patients. There is no difference in the mean amount of miR-1 between cancer patients and healthy patient populations. Question 2 (1 point) What is the response (or dependent) variable in the study? Question 2 options: The patient type (healthy patient or cancer patient) The average number of miR-1 fragments. The number of miR-1 fragments The average difference in the number of miR-1 fragments between healthy and cancer patient Question 3 (1 point) What is the predictor (or independent) variable in the study? Question 3 options: The average difference of number of miR-1 fragments between healthy and cancer patients. The number of miR-1 fragments. The patient type (healthy patient or cancer patient) The average number of miR-1 fragments. Question 4 (1 point) How many populations are being sampled? Question 4 options: 56 2 1 28 Question 5 (1 point) What is/are the population(s) being sampled? Question 5 options: The miR-1 fragments in colon cancer patient and the miR-1 fragments in healthy patients All the people with colon cancer, and people without colon cancer All the people in Western societies All the people in the medical study Question 6 (1 point) What is the appropriate type of t-test to use for these data? Question 6 options: single sample t-test independent (two) samples t-test paired t-test Variance ratio test

Explain how obesity can trigger insulin resistance.

how a diet high in saturated fat can contribute to insulin resistance.

Chronically elevated blood insulin levels and insulin resistance contribute to an increased risk for obesity.Group startsTrue or False