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Blurred Vision, Unexplained

Microscopic view of pancreatic islet cells. Courtesy Dr. José Sánchez Gonzales
Microscopic view of pancreatic islet cells. Courtesy Dr. José Sánchez Gonzales

What Is Type I Diabetes Mellitus?

T ype 1 diabetes mellitus (T1DM), also termed type 1A, is an inherited autoimmune disorder in which anti-islet autoantibodies destroy the islet cells of the pancreas that secrete insulin hormone. Type 1 diabetes mellitus was formerly called juvenile diabetes because it usually afflicts persons under the age of 25 years.

Loss of insulin production results in failure to metabolize glucose. Glucose is a simple sugar that is a required source of energy for the body, especially the brain and muscles.

Type 1 diabetes mellitus is characterized by sustained fasting blood glucose levels above 126 mg/dL (hyperglycemia) with subsequent loss of glucose from the body by removal through the urine (glucosuria) as the body attempts to lower blood glucose, and cell starvation that follows.

That is, while glucose accumulates in blood, the body cannot access it. Without insulin treatment, this disorder quickly produces coma and ultimately results in death. In fact, it is 5th leading cause of death in the United States.

Q: How does insulin work?

A: Insulin moves glucose from the bloodstream into body cells where it is used or reformulated for high energy storage. For example, muscles can use glucose for immediate work or store it in the form of glygogen for later work, depending on need. Healthy insulin production keeps an 8 hour fasting blood glucose level to less than 100 mg/dL. Upon eating carbohydrate food, glucose is digested and absorbed from the small intestine into the bloodstream which then raises blood glucose levels. The elevated level is controlled by prompt action of insulin to lower it to below 140 mg/dL  within 2 hours of eating.

Insulin does not work alone. The islets of Langerhans manage glucose in the body. The islets are specialized formations located on the outer surface of the pancreas. The islets are composed of two different types of cells known as alpha and beta cells. These cells make the competing hormones that keep blood glucose within a healthy range.

Alpha cells secrete glucagon to raise blood glucose levels by triggering the body to release stored energy in the form of glycogen. In the opposite, beta cells secrete insulin to lower blood glucose by opening body cells so that glucose in blood can enter. Without insulin, glucose cannot enter cells but remains in the bloodstream where it accumulates.

Insulin is also needed to move magnesium into cells from the bloodstream. On the other side, magnesium is needed to produce insulin. Insulin has other functions such as building muscle and helping regulate cholesterol which directly impacts the sex hormones, estrogen, progesterone, and testosterone.

Onset of symptoms usually occurs over a period of days or weeks, although beta cell destruction can begin years earlier. The SEARCH for Diabetes in Youth multicenter study, funded by the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH), has determined that based on data from 2002 to 2003, a total of 15,000 youth in the United States were newly diagnosed with type 1 diabetes each year. Non-Hispanic white youth had the highest rate of new cases of type 1 diabetes according to NIH.

Type 1A diabetes mellitus has become one of the most intensively studied autoimmune disorders. It is now possible to predict its development, beginning with HLA-encoded genetic susceptibility, followed by the development of a series of anti-islet autoantibodies.1

What Is Type I Diabetes Mellitus In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Liu E, Eisenbarth GS. Type 1A diabetes mellitus-associated autoimmunity. Endocrinology and Metabolism Clinics of North America. Jun 2002;31(2):391-410, vii-viii. [↩]

Dry Eye, Autoimmune (Keratoconjunctivitis Sicca)

gastrointestinal complications in diabetes symptom in gluten and celiac diseaseWhat Are Gastro-Intestinal Complications Of Type 1 Diabetes?

G astrointestinal complications of type I diabetes mellitus are functional or organic changes that result from diabetes affecting every organ of the gastrointestinal tract.

Q: How do gastrointestinal tract complications affect diabetes?

A: Impaired function of individual digestive organs in diabetes can significantly influence level of diabetes compensation and vice versa. On the other side, unsatisfactory diabetes compensation can result in manifestation of digestive problems.

The most frequent (55 to 75%) and the most serious clinical complication is diabetic gastroparesis characterized by impaired evacuation and motility of the stomach and small intestine. Gastroparesis results in nausea, vomiting, early fullness after eating and constipation.

Treatment is with prokinetics. These oral medicines help motility and transport of food in the esophagus, stomach and intestines and improve sphincter function to keep food from going backwards.

Gastroesophageal reflux and heartburn are other complications in diabetes. These are treated with antacids and acid reducing medications.

Various autoimmune disease interfere with digestion. One connection between diabetes mellitus and the gastrointestinal tract can be celiac disease.1

What Are Gastro-Intestinal Complications Of Diabetes In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Perusicova J. Gastrointestinal complications in diabetes mellitus. Vnitri Lekarstvi. May 2004;50(5):338-43. [↩]

Keratomalacia

Image From Gray's Anatomy. Courtesy Wikipedia.org
Image  of Pancreas From Gray’s Anatomy. Courtesy Wikipedia.org

What Is Pancreatic Insufficiency?

P ancreatic insufficiency is a disorder characterized by insufficient exocrine production of pancreatic enzymes for normal digestion of fats, proteins, and carbohydrates that results in maldigestion of these foodstuffs.

Pancreatic insufficiency also causes malabsorption of the fat-soluble vitamins: vitamin A, vitamin D, vitamin E, and vitamin K.

Q: What are the exocrine enzymes produced by the pancreas?

A: Exocrine enzymes produced by the pancreas include amylase for the digestion of carbohydrates, lipase for the digestion of fats, and protease for the digestion of proteins.

While lipases and amylase are secreted in the active form, proteases are secreted as pro-enzymes (need to be activated). Trypsinogen is converted to its active form trypsin in the duodenum by enterokinase, a protease secreted by the enterocytes (surface cells that line the duodenum), and trypsin in turn activates the other pancreatic proteases.1

Pancreatic enzymes are released by the pancreas into the internal pancreatic duct that empties into the common bile duct from which they are pumped through the Sphincter of Odi directly into the duodenum as needed. Tthe Sphincter of Odi is a strong circular muscle that controls the entrance of pancreatic enzymes into the duodenum.

After a meal, enzyme secretion into the duodenum increases quickly reaching peak output within the first 20 to 60 minutes, then decreasing to a stable level before reaching an interdigestive level at the end of the digestive period, that is, about 4 hours after meal intake.2

Medical treatment is with medication that contains enzymes to break down carbohydrates, fats, and protein in food at mealtime. This treatment is safe, effective, and has few side effects.

What Is Pancreatic Insufficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]
  2. Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]

Ocular Myopathy: definition

An impairment of musculature of the eyeball that is characterized by abnormalities of eye movement including difficulty initiating and maintaining eye movement and contact. Can result from magnesium deficiency. Click for full description.

Keratomalacia: definition

A severe non-inflammatory eye condition that is a late feature of Vitamin A Deficiency characterized by hazy, dry corneas becoming softened and denuded, which is then irreversible destroying the eyeball and causing blindness. Click for full description.