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Soriano S., Alonso-Magdalena P., Garcıa-Arevalo M., Novials A., & Muhammed S. J. (2012). Rapid insulinotropic action of low doses of Bisphenol-A on mouse and human islets of langerhans: Role of estrogen receptor b. PLoS ONE 7(2): e31109. doi:10.1371/journal.pone.0031109

Answer the following questions:

  1. What are the causes of type 2 diabetes?
  2. What is the relationship between insulin resistance and hyperinsulinemia?
  3. What are endocrine disrupters and their functions in our body?
  4. Provide some examples. How does concentration of glucose effect insulin secretion?
  5. Explain how data from article support or refute the hypothesis that endocrine disrupters can change insulin secretion.

Be sure to cite the article in text. Paraphrase key points from the article that support your answers.

comment 1

  1. What are the causes of type 2 diabetes?

There are different types of od glucose transporter that either are insulin-dependent or independent. For the purpose of this prompt, I will discuss on GLU-4. GLU-4 is a type of transporter that is found in the muscle and adipose cells. These transporters are insulin-dependent meaning insulin needs to be present for the activation of the cascade to occur within the membranous barrier. Since the body doesn’t produce enough insulin or is insulin resistant, then high amounts of glucose will be in the bloodstream.

Diabetes occurs when there are genetic and environmental conditions such as being overweight or having a sedentary lifestyle could contribute to this disease. A recent study in 2012 speculates that bisphenol -A, also known as BPA, could be one of the major cause of type 2 diabetes since its disrupts pancreatic B-cells function and induces insulin resistance (Soriano S, alt.,2012).

  1. What is the relationship between insulin resistance and hyperinsulinemia?

From the study, It was found that in mice, BPA was stated to regulate the release of insulin from the pancreas islets (Soriano S, alt.,2012). Although the body isn’t responding to the results of insulin, the pancreas will compensate by producing more insulin. This insulin will be released from the pancreas and travel to the blood but since the receptor in the membranous cell (muscle, liver, etc) is not functionally active, there will be a high in insulin in the blood. This is called hyperinsulinemia.

  1. What are endocrine disrupters and their functions in our bodies?

Endocrine disrupters can be natural or man-made that will would interfere with the body hormonal function. Its function acts as “hormone mimics” and trick our body into believing that they are hormones, whereas other EDCs block natural hormones from doing their job (Soriano S, alt.,2012). Some EDCs will either increase or decrease the levels of hormones in the blood by influencing how they are produced, broken down, or stored in our bodies (Soriano S, alt.,2012).

For instance, it is argued by these researchers from this study that BPA is an endocrine disruptor that will play a role in insulin resistance and triggers the activity levels a rapid of KATP channel which will function to sense any metabolic changes in the pancreatic beta-cell, thereby coupling metabolism to electrical activity and ultimately to insulin secretion (Copstead & Banasik, 2019).

  1. Provide some examples. How does the concentration of glucose affect insulin secretion?

The concentration of glucose in the extracellular fluid determines how much glucose intake will enter the cell (Copstead & Banasik, 2019).

Example 1: The person will consume a bowl of rice. With the use of amylase found in the mouth, it will enzymatically break down its micronutrient component into simple sugar, glucose. It will then need to be stored intracellularly as energy with the use of insulin mechanisms if there is a high level of glucose in the blood. Glucose will be stored as glycogen in muscle and liver cells.

Example 2: If the blood sugar level is too low, the pancreas will releases glucagon. Glucagon instructs the liver or muscle cells to release stored glucose, which causes blood sugar to rise

  1. Explain how data from article support or refute the hypothesis that endocrine disrupters can change insulin secretion.

According to this article, the tests found that the endocrine disruptor Bisphenol-A is responsible for insulin resistance (Soriano et al., 2012). The data to support this test was that researchers found that in mice, the presence of stimulatory glucose concentrations and low concentrations of BPA rapidly decrease KATP channel activity through estrogen receptor beta (mice), enhancing glucose-induced [Ca2+ ] signals insulin release. At the moment, this was only applied to rodent beta cells (Soriano et al., 2012). Thus, this results in a change in insulin secretion.

In humans, the receptors involved in the BPA regulation of KATP channel activity and insulin release is still undetermined and would need to conduct more studies (Soriano et al., 2012).


Soriano S, Alonso-Magdalena P, García-Arévalo M, Novials A, Muhammed SJ, et al. (2012) Rapid Insulinotropic Action of Low Doses of Bisphenol-A on Mouse and Human Islets of Langerhans: Role of Estrogen Receptor β. PLOS ONE 7(2): e31109.

Copstead, L. E., & Bansik, J. L. (2013). Pathophysiology. St. Louis, MO: Elsevier.

comment 2

  1. What are the causes of type 2 diabetes?

Bisphenol A (BPA) is a natural, manufactured compound utilized to create plastics and epoxy resins. It is being used as an auxiliary part in polycarbonate drink bottles and as covering for metal surfaces in food holders and bundling. The antagonistic impacts of BPA on human wellbeing are broadly questioned. BPA has been as of late connected with a wide assortment of clinical issues, and, correctly, it was recognized as a potential endocrine-upsetting compound with diabetogenic activity. A large portion of the clinical observational examinations in people uncover a constructive connection between BPA introduction, assessed by the estimation of urinary BPA levels, and the danger of creating type 2 diabetes mellitus. Clinical examinations on people and preclinical investigations on in vivo models demonstrate that BPA, for the most part at low dosages, may have a job in expanding type 2 diabetes mellitus formative hazard, legitimately following up on pancreatic cells, in which BPA instigates the disability of insulin and glucagon discharge, triggers hindrance of cell development and apoptosis, and follows up on muscle, hepatic, and fat cell work, setting off an insulin-resistant state. ( Alonso-Magdalena P, Quesada I, Nadal A (2011)

2. What is the relationship between insulin resistance and hyperinsulinemia?

The group of insulin resistance and hyperinsulinemia, hindered glucose resilience, variations from the norm of plasma lipids, and hypertension, presently regularly called the metabolic syndrome.
Hyperinsulinemia in the basal condition of any root produces far-reaching insulin obstruction. All tissues that have insulin receptor pathways will be influenced, including the pancreatic β-cell, and conceivably the brain. Inadequate insulin signaling at the β-cell hinders glucose-invigorated insulin discharge. A consistent state, basal hyperinsulinemia creates and continues insulin resistance, independent of where the pathology began. Hyperinsulinemia, insulin resistance, and disability of glucose-invigorated insulin discharge are entwined naturally. A single procedure (hyperinsulinemia) could create each of the three at the same time.
There are a few factors that add to insulin discharge. In the basal state, free unsaturated fat levels act partially to stimulate the arrival of insulin. Obese subjects have elevated levels of free unsaturated fats, and this may be a significant supporter of the hyperinsulinemia present in these patients. Basal insulin levels are such a substantial determinant of insulin affectability; it is critical to comprehend the various components that are driving the hyperinsulinemia in the basal state. It might be that the stimulus for basal hyperinsulinemia fluctuates by a patient and disease state. ( Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A (2006)

3. What are endocrine disrupters and their functions in our bodies?

Numerous synthetic compounds, both natural and human-made, may copy or meddle with the body’s hormones, known as the endocrine system. Called endocrine disruptors, these synthetic substances are connected with reproductive, brain, immune, and different issues. Endocrine disruptors are found in numerous regular items, including some plastic jugs and compartments, liners of metal food jars, detergents, fire retardants, food, toys, makeup, and pesticides. Some endocrine-disturbing synthetic compounds are delayed to break-down in the earth. That trademark makes them possibly dangerous after some time. An initiates a fast decline of the movement of KATP channels, a critical atom in the improvement discharge coupling of b-cells. Besides, the current work exhibits that ecologically applicable portions of BPA invigorated glucose-instigated insulin discharge in human islets, giving a reaction which is double the insulin discharge evoked by a stimulatory glucose concentration (Alonso-Magdalena P, Quesada I, Nadal A (2011)

4. Provide some examples. How does the level of glucose affect insulin secretion?

Insulin and glucagon are hormones discharged by islet cells inside the pancreas. They are both emitted in response to glucose levels, however, in inverse design. Insulin is ordinarily removed by the beta cells (a sort of islet cell) of the pancreas. The stimulus for insulin discharge is high blood glucose. Even though there is consistently a low degree of insulin emitted by the pancreas, the sum discharged into the blood increments as the blood glucose rises. So also, as blood glucose falls, the measure of insulin released by the pancreatic islets goes down.

5. Explain how data from article support or refute the hypothesis that endocrine disrupters can change insulin secretion.

The etiology of type 2 diabetes mellitus includes the acceptance of insulin resistance alongside the disturbance of pancreatic β-cell work and the loss of β-cell mass. Notwithstanding a hereditary inclination, way of life factors appears to have a significant role. Epidemiological examinations show that the expanded nearness of endocrine-disturbing chemicals (EDCs) in the earth may likewise have considerable domination on the incidence of metabolic diseases. Far-reaching EDCs, for example, dioxins, pesticides, and bisphenol A cause insulin resistance and adjust β-cell function in animal models. These EDCs are available in human blood and can aggregate in and be discharged from adipocytes. In the wake of binding to cell receptors and other targets, EDCs either mimic or block hormonal reactions.


Alonso-Magdalena P, Quesada I, Nadal A (2011) Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol 7: 346–353)

Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A (2006) The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance. Environ Health Perspect 114: 106–112

Alonso-Magdalena P, Quesada I, Nadal A (2011) Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol 7: 346–353

Dyachok O, Idevall-Hagren O, Sagetorp J, Tian G, Wuttke A, et al. (2008) Glucose-induced cyclic AMP oscillations regulate pulsatile insulin secretion. Cell Metab 8: 26–37

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