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Insulin works antagonistically with glucagon to control blood sugar levels. GHIF (growth hormone inhibiting factor – delta cells
Insulin is a polypeptide hormone that travels around the bloodstream. Most of the cells in the body carry receptors for the molecule in their cell membranes. Once the hormone has become bound to one of these receptors, the receptor gives a signal to the cell&apos;s interior. This signal leads to many enzyme controlled reactions which, in turn lead to changes in the metabolism of the cell. Many of the effects of insulin depend on the particular cell type in which it stimulates. However, in nearly all of the cells that have insulin receptors in their cell membrane, the binding of insulin to the receptors leads to increased glucose uptake of the cell. The two types of cells that are the main exceptions are the brain and the liver. However, this is only due to the fact that these cells are readily permeable to glucose, even in the absence of insulin. Liver cell membranes do contain insulin and glucagon receptors, but binding of the hormone to them affects cellular processes other than glucose permeability. The animation below illustrates the way insulin brings about the increase in glucose uptake Glucose enters the cells of the body through glucose transporter (GLUT) proteins which are embedded within the cell membrane. This is a process called facilitated diffusion. When insulin binds to it&apos;s receptor, the intracellular domain of the receptor changes shape slightly. This sets off a chain of reactions. These reactions serve to activate certain enzymes. As a result, more glucose transporter proteins are released from intracellular stores and move to the plasma membrane and become embedded within it.
Stimulating the uptake of glucose by the tissues Converting glucose to glycogen in the liver Increasing the production of fats and proteins
What goes wrong in diabetes? The body’s response to blood sugar requires the coordination of an array of mechanisms. Failure of any one component involved in insulin regulation, secretion, uptake or breakdown can lead to the build-up of glucose in the blood. Likewise, any damage to the beta cells, which produce insulin, will lead to increased levels of blood glucose. Diabetes mellitus, commonly known as diabetes, is a metabolic disease that is characterized by abnormally high levels of glucose in the blood. Whereas non-diabetics produce insulin to reduce elevated blood glucose levels (i.e. after a meal), the blood glucose levels of diabetics remain high. This can be due to insulin not being produced at all, or not in quantities sufficient to be able to reduce the blood glucose level. The most common forms of diabetes are Type 1 diabetes (juvenile onset, 5-10% of cases), which is an autoimmune disease that destroys beta cells, and Type 2 diabetes (adult onset, 90-95% of cases), which is associated with insufficient insulin. In either case, diabetes complications are severe and the disease can be fatal if left untreated. Insulin is the foundation for the management of insulin-dependent diabetes. Unfortunately, the use of insulin is not a cure nor without side effects. In certain parts of the world, it is not even available. Insulin is also not completely effective in preventing complications of the disease such as blindness, heart disease, kidney failure, etc. While millions of men, women, and children await a life without diabetes, let us hope that policy makers and the scientific community can converge on strategies that promote discovery for a cure.
Pre-diabetes: in USA estimated that 40% of people aged &gt;40 have pre-diabetes ie BGL increased but not at diagnostic levels. Increased risk of DM, cardiovascular disease, ?cognitive decline, risk of cancers (CDC 2004)
Blood sugar levels are dependent upon glucose uptake after meals and hepatic release of glucose between meals. The sugar released from the liver comes either from stored glycogen or production of glucose from lactate and amino acids. This production of glucose is largely responsible for stabilization of postprandial blood sugar levels. The hyperglycemia noted in type 2 diabetes partially results from lack of control over hepatic glucose formation due to resistance to insulin. It has recently become clear that part of this insulin effect occurs indirectly through insulin-sensitive receptors in the brain (more precisely, in the hypothalamus).
No evidence to support eating too much sugar leads to diabetes Obesity is key risk factor W:H ratio most useful predictor (women &lt; 0.80 ,men &lt; 0.95) Saturated fat is an independent risk factor Low fruit and vegetable intakes have been linked to higher HbA1c in general population (EPIC Norfolk study) Inactivity is an independent risk factor
Balance food intake with insulin (or oral agents) and activity to achieve blood glucose levels as near normal as possible. Achieve and maintain normal lipid (cholesterol) levels
Provide energy to reach and maintain short and long term body weight Reach and maintain normal growth and development in children and adolescents Prevent or treat complications Improve and maintain nutritional status Provide optimal nutrition for pregnancy
Diabetes mellitus and D inspidus
Submitted by: Dr. Kanwarpal Singh Dhillon
Diabetes mellitus is a chronic disorder of
carbohydrate metabolism due to relative or
absolute insulin deficiency
Diabetes is a life-long disease marked by high
levels of glucose in the blood
It can be caused by too little insulin, resistance to
insulin, or both.
Insulin (beta cells)
◦ stimulates the uptake of glucose by body cells thereby decreasing
blood levels of glucose
Glucagon (alpha cells)
◦ stimulates the breakdown of glycogen and the release of glucose,
thereby increasing blood levels of glucose
Glucagon and insulin work together to regulate &
maintain blood sugar levels
Enables glucose to be transported
into cells for energy for the body
Converts glucose to glycogen to be
stored in muscles and the liver
Facilitates conversion of excess
glucose to fat
Prevents the breakdown of
body protein for energy
Multitude of mechanisms
Uptake or breakdown
◦ Beta cells
1. Immune-mediated destruction of islets occurs
leading to B-islet cell dysfunction relative or
absolute deficiency of insulin.
2. severe pancreatitis in dogs
3. Insulin resistance due to
4.chronic use of glucocorticoids
5.pregnancy and diestrus .
In dogs ,progesterone causes release of growth
hormones leading to hyperglycemia which
develop insulin resistance.
◦ Obesity: 4 X more likely to develop DM
◦ Genetics ??
◦ Amyloidosis of the pancreatic cells
Factors lead to impaired insulin action in liver,
muscle and adipose tissue and β–cell failure
If some β–cell function exists, diabetes may be
• Occur in middle-aged dogs(7-9yr) and cats
• In dogs: female > Males
• In cats: Male> Female
• More susceptible dog breeds: Miniature Poodles,
Dachshunds, Schnauzers, Cairn Terriers, and
Prevalence increasing over time: aging population,
obesity, physical inactivity
There are two major types of diabetes:
◦ Type 1 Diabetes
◦ Type 2 Diabetes
Aetiology of DiabetesAetiology of Diabetes
Type One Diabetes
results when the body’s immune system
destroys its own beta cells in the pancreas.
No insulin production is then possible.
Type Two Diabetes
results from either
Insulin resistance (overweight patients)
Inadequate insulin production (lean
A combination of both
Insulin levels may be normal, elevated or
◦ Characterized by insulin resistance,
◦ Diminished tissue sensitivity to insulin,
◦ Impaired beta cell function (delayed or inadequate insulin
What is Insulin Resistance?
Condition in which the body does not utilise
Insulin resistance is the decreased response of the
liver and peripheral tissues (muscle, fat) to insulin
Insulin resistance is a primary defect in the
majority of patients with Type 2 diabetes
Characteristics of Diabetes
Type 1 Type 2
Normal or underweight
Little or no insulin
Low familial factor
Treated with insulin, diet
80% are overweight
Most have insulin resistance
Part of metabolic insulin resistance
Diet & exercise, progressing to
tablets, then insulin
Decreased resistance to bacterial and fungal
Develop prostatitis, bronchopneumonia, dermatitis
Emphysematous cystitis… Proteus,
Aerobacter aerogens, E. coli
Impaired chemotactic, phagocytic, antimicrobial
activity due to decreased neutrophilic function
Hepatomegaly due to lipid accumulation
In addition to high glucose levels, acutely ill
type 1 diabetics have high levels of ketones.
◦ As cells cannot get glucose, they burn fats as an alternate energy
◦ Ketones are produced by the breakdown of fat and muscle, and
are toxic at high levels
◦ Ketones in the blood cause a condition called "acidosis” or
“ketoacidosis" (low blood pH)
◦ Urine testing detects ketones in the urine
◦ Blood glucose levels are also high.
Develop frequently in dogs
Related to unique sorbitol pathway by which
glucose is metabolized in the lens leading to
Edema of lens and opacity.
Rare in cats.
• Based on persistent fasting hyperglycemia
• Normal fasting Glucose….75-125mg/dL
• In Cats stress induced hyperglycemia…. So take
• Serum glycosylated Hb or fructosamine
help to DDx stress induced hypergylcemia
Dogs and cats
BID dosing needed with 2 meals of equal calories
DOGS: 0.25-0.5 units/kg BID
Diet high in simple sugars should be provided.
In dogs with poor control of diabetes on NPH or
lente insulin use of basal insulin detemir should be
Starting dosage is 0.1U/kg , bid with
reassessment of clinical signs in 1 wk.
Treat DKA IV Continuous
SC q12h 8-14hr 6-12hr
Lente Pure pork Good initial
SC q12h 8-14hr 8-14hr
PZI 90% beef
“ SC q12h - 10-14hr
SC q12-24h 10-
Dog may be hospitalized for up to 24 hours
Food and insulin injection(s) will be given according to the
usual schedule at home (pet owner’s normal regime
This includes insulin injections, size, type and timing of
meals and exercise routine
A blood sample will be taken prior to feeding and insulin
Blood samples will then be taken every 1-2 (or 4 hours)
for up to 24 hours
Blood glucose will be measured in each of these samples
The blood glucose levels are plotted against time to produce a curve.
This curve indicates the changes in blood glucose levels after the
insulin is injected.
The highest blood glucose concentrations occur at
the time of each insulin injection
The lowest spot in the curve is called the nadir.
If the blood glucose nadir is >150mg/dl, the insulin
dose may be increased
If the nadir is less than 80mg/dl, the insulin should
A glucose nadir occurring 12 hr or longer after
insulin administration. indicates prolonged duration
of insulin effect
It looks like a bowl
The nadir, appears halfway between insulin injections
If the dog’s blood glucose does not go lower than 100
mg/dl or higher than 300 mg/dl during the observation
period, it means that the insulin doses and duration are
In cats ,Glargine is the initial insulin of choice.
It is used in combination with high protein and low
It Is associated with remission of diabetes and
discontinuation of insulin therapy in 80-90% cases
Sulfonylureas Glipizide @ 2.5mg,bid
Cats Glimepiride @2mg sid
Alpha-Glucosidase inhibitors acarbose in cats
@12.5-25mg,bid-tid in conjunction with diet
Therapy involves – 1. I/V fluids like RL for
correcting dehydration and acidosis.
2. giving regular insulin @ 0.2U/kg followed by
0.1U/kg regular at hourly interval.
3.once glucose level comes <250mg/dl then dose
of 0.5U/kg is given every 4-6 hr s/c.
Primary Goal – improve metabolic
Lipid (cholesterol) levels
CATS: low carbohydrate, high protein, mod-high
DOGS: low fat, high fiber
◦ >12% slowly fermentable , insoluble fiber or
>8% moderately fermentable fiber.
Royal Canin Diabetic HF
Royal Canin Calorie Control CC High Fibre (obese )
To encourage weight loss
To decrease insulin resistance induced by obesity
Diabetes insipidus is a condition characterised by
PD,PU and excretion of large amount of hypotonic
It occurs either due to low level of ADH in the
body or due to impaired response of renal tissue
to normal level of ADH in body.
Etiology & classification
Central diabetes insipidus: reduced secretion of ADH:
◦ also known as hypophyseal form
◦ Develops due to some lesion in hypothalamus
◦ 1. pituitary neoplasms,
◦ 2. cyst
◦ 3. inflammatory granuloma
◦ 4.trauma etc.
Nephrogenic diabetes insipidus: Kidney fails to
respond to normal secretion of ADH.
PU/PD: Passing large volume of hypotonic urine
Urine osmolality is decreased below normal
plasma osmolality (approx 300 m Osm/kg) even
during water deprivation.
History: chronic PU/PD that does not respond to dehydration and is not
due to primary renal disease
Water deprivation test
ADH response test
◦ Bladder is emptied and water and food are withheld for 3 to 8 hours
◦ Urine and plasma osmolality is deterimined
◦ At the end: If urine sp gr > 1.025: only a partial ADH deficiency or with
antagonism of ADH action by hypercortisolism
◦ Little change in sp gr : Complete lack of ADH:
Measure urine sp gr. at the start (Normal sp gr of dog
urine: 1.020 to 1.040)
Put 2-4 drops of desmopressin acetate in the
Empty the bladder at 2 hours
Collect urine again at 4,8,12, 18 and 24 hours and
measure sp gr
Sp gr. peaks at > 1.026 in animals with a primary
ADH deficiency, but show little change with
nephrogenic diabetes insipidus
After water deprivation:
◦ >3 normal animals
◦ 1.6-3 in animals with moderate ADH deficiency
◦ <1.8 in animals with severe ADH deficiency
After ADH administration
◦ > 2 in animals with primary ADH deficiency
◦ Between 1.1-2 in partial ADH deficiency
◦ < 1.1 in unresponsive ADH cases
Diabetes mellitus: glycosuria and high urine sp gr
Chronic nepthritis : usually associated with renal
Desmopression acetate (synthetic analog of ADH)
◦ 2 drops on the nasal mucosae or conjunctivae SID to
BID for life long
Caution: cardiac patients.
Do not restrict water.