Post-1:
Poop test can tell if you are diabetic, say docs
TNN | Mar 3, 2016, 07.09 AM ISTSymptoms:
1. Sudden weight loss;
3.Too much thirsty or Poly-Dypsia
4.Too much hungry or Poly Phagia
6.Ketoacidosis, a condition at which ketone bodies are circulated all over the body tissues. This symptom is the immediate consequence in Type-1 D.M
7. Because sugar is excreted more in urine mostly the urinals or toilets is swarmed with
ants and flies
Diagnosis:1.At fasting, the test result will show the reading equals to or above 130 mg/dl
2. After the loading of a 75gm oral glucose dissolved in 300 ml water in a 12 hr fasting period if the test reading after a 2 hr test is equaled or above will confirm D.M
INSULIN
CHEMISTRY: Insulin by itself is a polypeptide composed of two chains of aminoacids one below another as a double row linked by disulfide (sulfur-sulfur) bonds between cysteine residues as you can see in its molecular structure shown below. It contains a total number of 51 amino acids.
When Insulin binds to the cell receptors which is a tyrosine kinase present on the cell wall then the cell secretes transporters out to the cell membrane and these transporters in the presence of insulin carry glucose inside the tissue cell to metabolize it.
Type-1: Fully insulin-dependent as there is no secretion of insulin at all and daily intake of insulin is the primary treatment. A maximum of 10% of the people is affected by this type. Very rarely its by hereditary and by genetic transfer. It is mostly by body self-defending system otherwise known as autoimmunity as the pancreas of these patients are found with antibodies damaging beta islets.Type-2: Partly Insulin-dependent or Fully Insulin Independent as insulin secreted not sufficiently in this type for the cells to respond.Various oral antidiabetic drugs with insulin if needed. Almost 90% of the people are suffering by this type. These types are mostly hereditary and genetic transfer.
Types of Insulin-A Brief
1)Short-Acting:-Insulin Lispro (Humalog) and regular (Humulin)
2)Medium Acting:-Isophane insulin suspension (NPH), and insulin zinc suspension
3)Long-Acting:-Insulin zinc suspension Extended(Ultra Lente)
Toxicology
1)Hypoglycemia (a sudden lowering of blood sugar)2)Insulin Allergy
3)Insulin Antibodies
4Lypodystrophy-a change in the fatty tissue surrounding the injection site
Pharmacokinetics
Insulin: The Pharmacokinetics of insulin comprises of its absorption from the site of administration, distribution including attacked and neutralized by circulating antibodies, degradation, and excretion. The distribution and metabolism of insulin administered from outside that are exogenous follow exactly the same as how the endogenous insulin is done. But in certain circumstances, the exogenous insulin distributed may be resisted by produced and circulating antibodies which may cause insulin resistance may alter the kinetics, otherwise it cannot be actively changed. The use of preparation with low immunogenicity may reduce this variation.
The absorption process the details are still unknown is influenced by many variables some of which can be controlled, and thereby the differences can be reduced between individuals. Besides this, the volume and size of the doses, the timing between individual doses, the site of injection, and the type of insulin preparation and the permeability and blood flow of the injected tissue also influence the absorption.
Serum insulin may peak up to one hour after the injection, of soluble insulin into the thigh Vs into the abdominal wall.
Pharmacodynamics
Insulin after underwent to some kinetic process insulin reaches the site of its actions mainly the cell receptors. Once it got the reception well at the receptors (tyrosine kinase)on the cell membrane (remember insulin does not enter into the cell) the cells from inside its compartment elude a kind of proteins known as the sugar transporters or carriers to carry the glucose molecules inside the cells. This will happen only in the presence of insulin attached well to the cell receptors without any resistance. The cells metabolize the glucose to produce energy and other needed molecules and the remaining will be converted into Glycogen and Fat for storage into muscles and adipose tissues.
Excretion
Insulin after consumption by the tissues as a remaining portion cannot either circulate in the system or re-enter into its original place of production as it is harmful if it remains in the body hence the body eliminates it as unchanged in the urine by kidneys.
Oral Anti Diabetics-A Brief
1.Sulphonylureas:-Chlorpropamide, a first-generation drug (Diabinese);
Glibenclamide, a first-generation drug (Dionil)
Glibenclamide, a first-generation drug (Dionil)
Tolbutamide, a first-generation drug (Orinase)
Glyburide, a second-generation drug(Micronase)
Glipizide, a second-generation drug, high potent (Glucotrol)
Glimepiride, a second-generation drug, high potent (Amaryl)
MECHANISM: They stimulate the release of endogenous insulin from the pancreas and increase the binding strength of insulin to its target receptors
TOXICITY:1.Hypoglycemia a condition in which the blood glucose level is abnormally low due to an overdose
2.Gastro-intestinal distress
3.Pruritus
4.Nausea
5.Agranulocytosis and aplastic anemia (rare)
Metabolism and Excretion: These agents are metabolized in the liver and excreted in the urine
Metabolism and Excretion: These agents are metabolized in the liver and excreted in the urine
2.Biguanides
1.Metformin (Glucophage) and
2.Phenformin
Mechanism: It is assumed as glycolysis in the peripheral tissues and reduces hepatic gluconeogenesis. Metformin is contraindicated in Liver and Kidney diseases, in Cardiac arrest, and chronic hypoxic lung disease. It is also advised to stop metformin prior to the radiological procedure involving the usage of iv iodinated contras medium to avoid possible renal failure.
Excretion:
Metformin is excreted unchanged by kidneys without metabolized in the liver Toxicity:1. Lactic acid elevation in the blood as is excretion is blocked 2.Diarrhea, nausea, and stomach upset.
Excretion:
Metformin is excreted unchanged by kidneys without metabolized in the liver Toxicity:1. Lactic acid elevation in the blood as is excretion is blocked 2.Diarrhea, nausea, and stomach upset.
3.Decreased absorption of Vit.B-12, and Folic acid in long time use
3.Alpha Glucosidase Inhibitors: 1.Acarbose (Glucophage):Mechanism: This drug delays the absorption of glucose from the GI tract.
Metabolism and Excretion: Acarbose is metabolized within the GI tract by intestinal bacteria and digestive enzymes and excreted in stools and some amount which entered in the system may be excreted unchanged by kidneys in the urine.
Toxicity: GI distress, bloating and diarrhea
4.Thiazolidinediones:
The use of these groups is now under consideration as rosiglitazone is withdrawn from the market for its serious hepatitis side effects. The other members of this group such as pioglitazone(Actos), rosiglitazone(Avandia ) are still used in many countries.
Vidaglyptin
It is a Dipeptidyl peptidase (DPP) inhibitor class of medicine. It inhibits the enzyme and thereby promote the action of Glucagon-Like Peptidase and Gastric Inhibitory Polypeptide(GPP) and thereby promoting the insulin secretion in the pancreas
In the news:-Energy Healing May Help Treat Type-1 Diabetes Patients, Says A New Study
Now a new study by TAG-VHS Diabetes Research Centre shows a form of "metaphysical energy therapy" that may help those afflicted with Type 1 diabetes come out of their life-long dependence on medicines. The medical paper published in the Journal of Diabetes Mellitus (JDM), a peer-reviewed medical journal in the US, is a major step forward in juvenile diabetes research, says Dr. Krishnaswami, the lead author of the paper. "This is a paradigm shift in research where we have introduced the concept of energy medicine and used it to heal imbalances in the body. In our study we found that the use of this alternate form of medicine helped people reduce their dose of insulin and one went off it completely," he adds. Dr. Krishnaswami, however, says the study is at its nascent stage and requires in-depth analysis before a treatment procedure can be recommended.
Type 1 diabetes usually occurs in children below the age of 15 years in which the body's immune system attacks a part of its own pancreas, mistaking the insulin-producing cells in the pancreas as foreign, and destroys them. The DAMM therapy that was tested on 15 people, with recent and longstanding insulin-dependent diabetes mellitus showed significantly improvement in fasting C-peptide levels in six cases. "In this study, with this new mode of treatment, we could find out the improvement in fasting C-peptide levels and weight of the subjects, with minimum settings of DAMM Therapy and medium dosage of insulin intake," says Dr. Krishnaswami.
Type 1 diabetes usually occurs in children below the age of 15 years in which the body's immune system attacks a part of its own pancreas, mistaking the insulin-producing cells in the pancreas as foreign, and destroys them. The DAMM therapy that was tested on 15 people, with recent and longstanding insulin-dependent diabetes mellitus showed significantly improvement in fasting C-peptide levels in six cases. "In this study, with this new mode of treatment, we could find out the improvement in fasting C-peptide levels and weight of the subjects, with minimum settings of DAMM Therapy and medium dosage of insulin intake," says Dr. Krishnaswami.
Therapy is said to infuse and transfer healing energy from the environment (cosmos) through the therapist, to the patient using acupuncture.
Lack of access to expensive insulin, limited health professional expertise concerning childhood diabetes, and extreme poverty can result in misdiagnosis of the disease which may lead to loss of vision, end-stage renal failure, and severe neuropathy in the 20s or even earlier. With the advent of this the new study, which reports no apparent side-effects in the treatment, the cost of treatment can be greatly reduced, believes Dr. Krishnaswami. "Though the incidence of Type I diabetes is much lower in India as compared to the western countries, the numbers are still sizeable in our country," he added.
Located inside the VHS campus, TAG-VHS, a 40-bedded hospital, was established in 2011. It uses a range of "non-invasive procedures" based on energy medicine, which Krishnaswami says science is now recognizing.
Gut bacteria could help understand diabetes better
Could the trillions of bacteria in our gut hold the key to understanding why some people get diabetes and also offer a potential cure?
To find out, doctors in India and Denmark are collecting samples of stool from about 900 people in both countries, extracting DNA from it and studying it — to figure out for instance, if Indians have more aggressive gut bacteria leading to insulin resistance, or how diverse the bacteria are, and how they are affecting the health of people.
The study called ‘Microbdiab’— jointly funded by the Danish government and the department of biotechnology, Government of India — is a collaboration between three organizations in India, including Dr. Mohan’s Diabetes Specialties Centre, as well as the University of Copenhagen.
The stool samples are from people who are pre-diabetic, diabetic, and normal — 450 samples in each country.
Oluf Pedersen, professor of molecular metabolism and metabolic genetics, faculty of health and medical sciences, University of Copenhagen, Denmark, says, “Gut bacteria produce thousands of compounds that enter the bloodstream, are circulated to all organs, and have an impact. Studies have shown they impact the brain too. They can cause diabetes or lead to obesity.
Different disorders
They have an enormous capacity for inducing different disorders. Is there a role for gut bacteria in the development of pre-diabetes and type 2 diabetes and is there a universal gut bacteria that are contributing to causing diabetes worldwide — these are some of the questions we are studying,” said Prof. Pedersen.
Prof. Pedersen was presented the 25th DMDSC Gold Medal Oration Award on Wednesday. Research has indicated that certain gut bacteria are linked to type 2 diabetes, but whether they are innocent bystanders or part of the causation is yet to be explored, he said.
The Microdiab study began a year ago, and is expected to come up with findings in about six months or so, said R. M. Anjana, joint managing director of the Centre.
Indians could have less good bacteria or less diverse bacteria or more bad bacteria, said V. Mohan, chairman of the Centre.
The Indian diet could be a contributing factor, as diet affects gut bacteria.
Prof. Pedersen, in previous research, has been able to show that those who have more diverse gut bacteria are protected from various diseases like type 2 diabetes and obesity, he said.
Eventually, the goal would be to develop prebiotics or probiotics, to help good bacteria flourish so as to prevent type 2 diabetes, said Prof. Pedersen.
His research has shown that even monozygotic twins have different gut bacteria.
Elaborating on his experiments, he said injecting the gut bacteria of an obese mouse into a germ-free mouse could make the latter obese.
Injecting a lean mouse’s gut bacteria into a germ-free mouse led to the mouse remaining lean — showing that gut bacteria could influence obesity
900 stool samples will be taken from people who are pre-diabetic, diabetic and normal in India and Denmark
