endocrine pancreas & carbohydrate metabolism

alpha cells

produce glucagon

beta cells

produce insulin

insulin

• release stimulated by increased entry of glucose into beta cells (increased plasma glucose)

• polypeptide; short half-life

• only hormone that actively drives glucose entry into cells

glucagon

• polypeptide; short half-life

• decreases glucose utilization (inhibits glycolytic enzymes)

• increases generation of glucose and alternate energy sources (ex. lipolysis, gluconeogenesis, glycogenolysis)

• secretion increased in the absence of insulin, during low plasma glucose, fasting states

IDDM (type 1)

• inability of pancreatic beta cells to produce insulin (true insulin deficiency)

• more common in:

  • young to middle-aged patients

  • dogs

NIDDM (type 2)

• lack of tissue responsiveness to circulating insulin (relative insulin deficiency)

• most common in:

  • older, overweight patients

  • cats > 8 yrs old (takes time to develop disease)

• obesity is a major contributor (excess adipose tissue inhibits insulin)

• secondary to other endocrine diseases (ex. cushing’s disease, acromegaly)

• damage to beta cells may eventually lead to IDDM

diabetic ketoacidosis (DKA)

in the absence of insulin + excess glucagon, excess fat breakdown results in formation of acidic ketones → very serious emergency

insulinoma

• excess circulating insulin

• functional tumor of pancreatic beta cells → secrete insulin regardless of plasma glucose level

• common in ferrets 4-6 years old

insulin effects

• increases glucose uptake and utilization → decreases plasma glucose

• store energy (synthesize proteins, fats, glycogen)

• inhibits synthesis of alternate energy sources (ex. breakdown of fats, proteins)

• inhibits glucagon secretion from alpha cells

• promotes K+ intake into cells (glucose-K+ symporter)

“diabetogenic” hormones

• some hormones can have diabetes-like effects or cause DM

  • typically by promoting insulin resistance and/or inducing metabolic imbalances similar to diabetes

• examples:

  • cortisol

  • growth hormone

  • catecholamines

• complicate treatment of DM

DM common clinical signs

• polyuria/polydipsia (PU/PD)

• weight loss (breaking down muscle & fats)

• appetite changes

laboratory abnormalities (diabetes)

• hyperglycemia

• glucosuria (glucose in urine)

• lipemia (hyperlipidemia) - ↑ fats in blood

• dilute urine (low specific gravity)

why is exercise recommended as part of treatment for diabetes?

• lowers blood glucose levels

• lowers insulin requirements

  • muscle tissue utilizes glucose via non-insulin dependent means → during exercise, muscle cells move GLUT4 transporters to cell surface without insulin

• promotes lean body mass

  • resting muscle tissue utilizes glucose via GLUT1

  • low fat stores decrease availability of ketone sources

fructosamine level

• measures glucose irreversibly bound to plasma albumin

• indication of overall plasma glucose for past ~3 weeks

glucose curve

• measure plasma glucose level over time + in response to insulin administration

• most critical monitoring tool

  • determines adequacy of insulin dose

  • helps determine dosing interval

  • ensures insulin dose is not too high

• best method to assess efficacy of patient’s insulin dose

somogyi effect

• insulin overdose results in hypoglycemia → stimulates release of counter-regulatory hormones (body panics and overcompensates) → hyperglycemia, complicated by lack of insulin

• aka rebound/paradoxical hyperglycemia

insulinoma symptoms (major)

• lethargy, weakness, collapse

• neurologic

  • disorientation

  • ataxia

  • seizures

• early on, may be intermittent as long as body can compensate for hypoglycemia