Insulin Resistance and Exercise Essay

Without insulin there to make this happen, excess glucose remains in the blood if it’s not used by the muscles. Continued stress responses over time can eventually cause the uptake of glucose into the cells to be hindered, thereby creating a diabetic condition.

Diabetes occur when there is a combination of inadequate secretion of insulin by the pancreatic beta cells and the peripheral insulin resistance. Insulin resistance leads to a reduced glucose transport into the muscle cells, increases both hepatic glucose production and breaking down of fats because it has been attributed to the elevated level of free fatty acids and proinflamatory cytokines in the plasma.1

Insulin resistance is the first physiological change occurring in type two diabetes. In these type two diabetic patients, insulin is unable to move glucose into liver, kidney and muscle cells although insulin is able to attach properly to the cell surface receptors. In order to rectify this, most patients with type two diabetes start secreting normal to very high levels of insulin, which can initially overcome this resistance. After a while, the pancreas cannot keep up with this high insulin production and the cells become resistant to glucose intake. Persistent hyperglycemia or high blood glucose levels are not desirable since this causes damage to the beta cells of the pancreas that produces the insulin hormone. This damage to beta cells further hampers insulin synthesis and patients at this stage are categorized as full-blown diabetic. Such patients consistently show a hyperglycemia state even after hours of fasting ( Hinkle & Cheever,

Insulin is a hormone that is produced from what is known as the “islets of Langerhans”, discovered by German Histologist Paul Langerhans, and is required for the utilization of glucose in muscle cells for energy. If the muscles are deprived of glucose for energy conversion, the muscles begin to utilize fat for energy (Roth). This however has toxic side effects, such as the production of high blood levels of Ketone bodies or otherwise known as Acetone. In high quantities, Acetone will accumulate in the blood, leading to brain damage and the possibility of brain death (Roth).

In type 2 diabetes a person’s body produces insulin, but the pancreas does not produce enough insulin to maintain bodily functions or the body cannot use the insulin the way it is supposed to. When the body is unable to use insulin properly it is known as insulin resistance. “When there isn’t enough insulin or the insulin is not used as it should be, glucose (sugar) can’t get into the body’s cells” (WebMD, n.d.). When this happens glucose builds up in the blood and is not absorbed by the cells, which causes the body to not function properly. Some of the subsequent damage that can develop as a result of this

The insulin signaling cascade is initiated when insulin binds to insulin receptors located on the cell 's surface. The insulin receptor has four subunits: two alpha subunits located on the outside of the cell and two transmembrane beta subunits (3 & 4). When insulin binds to the alpha subunit receptors, it transmits a signal across the plasma membrane and activates tyrosine residues that are attached to the beta subunits. The activation of the tyrosine residues causes it to autophosphorolate and then phosphorolate other proteins that also have tyrosine residues attached to them. These phosphorylated proteins then move on to trigger cellular responses such as translocation of GLUT4 vesicule to the cell membrane. The vesicule becomes a transporter to allow glucose to come into the cell so that it can continue on and be stored as glycogen (3).

Is a result of the body’s immune system attacking the insulin producing beta cells of the

The organs involved include the liver, muscle, fat cells, liver, alpha and beta cells of the pancreas, GI tract, kidney, and brain. While the liver and muscle ideally increase glucose uptake in the fed state when insulin levels are high, with type 2 diabetes this is impaired. To further exacerbate the hyperglycemic condition, the liver not only fails to properly exhibit glucose uptake, but it actually over produces more glucose and thereby creates a cycle of glucose accumulation and further production. While this is occurring in the muscle and liver, fat cells have accelerated lipolysis. The lipolysis results in an increase in plasma free fatty acids (FFAs), which then in-turn impairs both first and second phase insulin secretion and can lead to excess fat deposition in the liver and muscle, contributing further to impaired insulin production. At the GI tract, gastric inhibitory polypeptide becomes resistant and loss of GLP-1 occurs. With impaired GLP-1, insulin resistance is again further enabled and hyperglycemia can become more profound. This occurs because glucagon suppression from the pancreatic alpha cells post meal does not occur as it would under normal circumstances, thereby enabling even more hepatic glucose production. While theories are not completely conclusive, insulin resistance in the hypothalamus may contribute to excess intake thereby contributing to additional glucose in the circulation. Finally, the kidney also plays a role in glucose dysregulation as it increases glucose reabsorption. All of these discussed mechanisms ultimately contribute to hyperglycemia and chronic hyperglycemia itself contributes to impaired beta cell function (DeFronzo,

Type one diabetes relates to ATP in several ways. The impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetes patients of insulin treatment will have several consequences. For starters, a withdraw of it can result in an increase in plasma glucose, branched chain amino acids, and nonesterified fatty acids. Also it decreases muscle mitochondrial ATP production rate. Insulin action per second can stimulate muscle mitochondrial function. Overall, cells rely on ATP, which relies on glucose, so it is important for a type one diabetic to maintain proper glucose levels. ( “Effects of Insulin Deprivation on Diabetes Patients” 1).

From recent research, it is hypothesized that insulin signaling in the cell can be influenced by acylcarnitines through a pro-inflammatory mechanism, causing insulin resistance (10). Although there is no direct correlation between insulin signaling and acylcarnitines, it is the aim of this study to determine the role of acylcarnitines in muscle insulin resistance. The behavior of acylcarnitines is a necessary component for connecting inefficient β-oxidation, oxidative, glucose response and inflammation.

Insulin causes cells in the liver, skeletal muscles, and fat tissue to absorb glucose from the blood.

Diabetes mellitus, commonly known as diabetes, is a metabolic disorder characterized by chronic high blood sugar levels. It is caused by an absolute or functional deficiency of circulating insulin, resulting in an inability to transfer glucose from the bloodstream into tissues where it is needed as fuel (Ahmed, Laing and Yates 2011). The disruption in the metabolism of carbohydrates, fats and proteins interferes with the secretion or action of insulin, which plays a vital role in the metabolism and utilization of energy from the nutrients especially carbohydrates. Insulin is produced in the pancreas and secreted in the gastrointestinal tract in the response to high blood sugar levels after ingestion of a substance (REFERENCE).

The IL-1β ELISA value demonstrated that the diabetic group (2228.18±183.187 pg/ml) was lower than the control group (2660.67±97.967 pg/ml). In contrast, the diabetic group supplemented with whey protein (2954.33±388.655 pg/ml) was very high than the diabetic group (2228.18±183.187 pg/ml) (Fig. 2). This study showed also that there is

When food reaches the digestive track, it transforms into glucose. That is a simple sugar. It is absorbed by the stomach and intestine and then it enters to the blood stream. When it is in the blood stream, the sugar level of our body rises. This gives signals to the pancreas, resulting in the liberation of the hormone called insulin. This hormone is very important because it helps glucose to reach important parts of the human body, such as the liver, muscles and adipose tissue or fat. It is also necessary because it helps to maintain sugar levels of our body. When the Pancreas does not produce insulin, the blood sugar level rises and glucose cannot reach the liver, muscle, and adipose tissue. This defect is called diabetes. The international Expert Committee in their article “International Expert Committee Report On The A1c Assay In The Diagnosis Of Diabetes” states that “Diabetes is a disease characterized by abnormal metabolism, most notably hyperglycemia, and an associated heightened risk for relatively specific long-term complications

Reactive hypoglycemia, a rare form of hypoglycemia, increases insulin levels after the consumption of excess carbohydrates, leading to a drop in blood glucose levels. This differs from conventional hypoglycemia where blood glucose drops several hours after a meal, but can easily be returned to normal by the consumption of food. Reactive hypoglycemia can cause fatigue, dizziness, shakiness, and in extreme cases, a coma. Although no effective treatments exist, glucagon, a peptide hormone derived from pancreatic alpha cells, seems to reduce symptoms. In the proposed experiment, the effectiveness of glucagon relative to a regimen of dietary control, exercise, and Acarbose will be tested on Zucker-diabetic-fatty (ZDF) rats (Rattus rattus). Three