Arfazetin - natural tea for type 2 diabetes treatment

PRODUCT DESCRIPTION

100 g species include: blueberry shoots - 20.0 g bean pods - 20.0 g, rhizomes with roots of eleuterococus - 15.0 g, dog rose fruit - 15.0 g aerial parts of Horsetail - 10.0 g aerial parts St. Johns Wort - 10.0 g, chamomile flowers - 10.0 g.

DESCRIPTION OF PREPARATION
Fragments of different shaped leaves, flowers, stems, shoots rhizomes and roots, fruit passing through the sieve hole diameter of 7 mm. Color: green-gray with pale yellow inclusions, brown-gray, cream, yellow-gray, red, orange brown, reddish, brown and white. Weak, flavoured smell. - weak flavor.

PHARMACEUTICAL FORM

Herbal tea. vegetable.

  PHARMACOTHERAPEUTIC GROUP AND ATC CODE

Vegetable hypoglycemic remedy HA10BX

PHARMACOLOGIC PROPERTIES

Plants of the species composition ARFAZETIN contain volatile oil, flavonoids, coumarins, polysaccharides, minerals, organic acids, tannins, alkaloids bitter substances, resins and other biologically active substances.
This complex set of biologically active substances possess hypoglycemic type II diabetes, allowing , into a number of cases to decrease peroral nictemeral antidiabetic dosage, increases glucose tolerance. In type I diabetes there was no significant hypoglycaemic effect.

Indications

Type II diabetes mild and medium form as monotherapy and in complex therapy.



 DOSAGE AND METHOD OF ADMINISTRATION

Put 5 g (1 dessert tbsp)of herbs in an enamel pot, add 200 ml (1 cup) of boiling water, cover with lid and leave in the water bath for 15 minutes. The infusion should be cooled to room temperature for 45 minutes, filtered, the residue is squeezed and added to the filtrate. Infusion volume brought to 200 ml by adding boiling water. Intern. Adults given warm infusion:  get 1/3 to 1/2 cup 2-3 times a day 30 minutes before meals. Children depending on AGE - from 1dessert spoon  to 1/4 cup of warm infusion 2-3 times a day 30 minutes before meals. Before administration shake the infusion.
The duration of the treatment is 20 to 30 days. After a 10-15 day pause course of treatment is recommended to repeat. For 1 year there should be 3-4 courses.

SIDE EFFECTS

In case of hypersensitivity to the components of individual species are possible allergic reactions. If the adverse development takes place,  the administration should be interrupted.
 
CONTRAINDICATIONS

Hypersensitivity to the active substance in the composition of biological species.

OVERDOSE

Cases of overdose have not been reported.

WARNINGS AND SPECIAL PRECAUTIONS FOR USE

During pregnancy and lactation
The drug should be administered , during pregnancy and lactation only in situations that potential benefits to the mother outweigh any potential risk to the fetus or infant.

Influence on ability to drive and use machines

The drug does not affect psychomotor speed reactions, so it can be used by people  who drive or handle potentially dangerous machinery.

Interactions with other drugs

  Complex therapy of diabetes may contribute to decreasing the dose peroral hypoglycemic remedies. Other clinically relevant interactions with other medicinal preparation were not reported.

Appearance, packaging

  50 g bags of white or brown paper or  filter paper. 1 bag with the administration instruction is placed in carton folding box.

STORAGE

Store in a dry place, protected from light at 15 to 25 C. Keep out of children.

SHELF LIFE

Two years. Do not use after the expiration date indicated on the package.

LEGAL STATUS

Without a prescription.

FDA Approves Invokamet (canagliflozin/metformin) for Type 2 Diabetes

RARITAN, N.J., August 8, 2014 – Janssen Pharmaceuticals, Inc. announced today the U.S. Food and Drug Administration (FDA) has approved Invokamet, a fixed dose therapy combining canagliflozin and metformin hydrochloride in a single tablet, for the treatment of adults with type 2 diabetes.

Invokamet provides the clinical attributes of Invokana (canagliflozin), the first sodium glucose co-transporter 2 (SGLT2) inhibitor available in the United States, together with metformin, which is commonly prescribed early in the treatment of type 2 diabetes. Invokamet is the first fixed-dose combination of an SGLT2 inhibitor with metformin approved in the United States.

"Invokamet combines, in one tablet, two complementary therapeutic approaches proven effective for managing type 2 diabetes,” said Richard Aguilar, M.D.*, Medical Director of Diabetes Nation.
"Canagliflozin works with the kidney to promote the loss of glucose in the urine, whereas metformin decreases the production of glucose in the liver and improves the body’s response to insulin."

Invokamet is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus who are not adequately controlled by treatment that includes either canagliflozin or metformin, or who are already being treated with both canagliflozin and metformin as separate medications. Invokamet should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis. Study results demonstrated that administration of Invokamet was equivalent to co-administration of corresponding doses of canagliflozin and metformin as individual tablets.

Invokamet will be available in tablets containing canagliflozin 50 milligrams (mg) or 150 mg, and metformin 500 mg or 1000 mg. The recommended dosing is twice daily. The prescribing information for Invokamet also contains a boxed warning for lactic acidosis, a rare, but serious complication that can occur due to metformin accumulation.

"As with Invokana, Invokamet provides adults with type 2 diabetes an oral therapy that lowers blood sugar and is also associated with reductions in body weight and systolic blood pressure," said Jimmy Ren, Ph.D., Therapeutic Area Lead, Metabolics, Medical Affairs, Janssen Pharmaceuticals, Inc.
"The available doses of Invokamet allow physicians to tailor therapy for individual patient needs and offer an alternative for patients who may be able to reduce the number of tablets they take each day."

In March 2013, the FDA approved canagliflozin -- Invokana -- as a single agent, and it is the number-one branded non-insulin type 2 diabetes medication newly prescribed by U.S. endocrinologists. It is also the second most common branded therapy prescribed by primary care physicians when adding or switching therapies in patients. Since its launch, more than one million prescriptions have been written for Invokana.

The co-administration of Invokana and metformin has been studied in six Phase 3 clinical studies that enrolled 4,732 patients with type 2 diabetes. The Phase 3 studies evaluated Invokana in combination with metformin compared to metformin alone or to metformin plus another diabetes therapy. The studies were part of the comprehensive global Phase 3 program for Invokana that enrolled 10,285 patients, one of the largest clinical programs in type 2 diabetes submitted to health authorities to date. The Phase 3 studies showed that the combination of Invokana and metformin lowered blood sugar and, in pre-specified secondary endpoints, was associated with significant reductions in body weight and systolic blood pressure.

In two studies comparing Invokana plus metformin to current standard treatments plus metformin – one studying sitagliptin and the other studying glimepiride – Invokana dosed at 300 mg provided greater reductions in A1C levels and body weight than either comparator. A1C is the percent of red blood cell hemoglobin with glucose attached to it and an indicator of average blood glucose over the previous two to three months. In the two studies, the overall incidence of adverse events was similar with Invokana and the comparators.

Results from the Phase 3 studies showed that the most common adverse events with Invokana are female genital mycotic (fungal) infections, urinary tract infections and increased urination. These specific adverse events were generally mild to moderate in intensity and infrequently led to discontinuation in Phase 3 studies. The most common adverse reactions due to initiation of metformin, as noted in the prescribing information for that medication, are diarrhea, nausea/vomiting, flatulence, asthenia, indigestion, abdominal discomfort, and headache. Hypoglycemia does not occur in patients receiving metformin alone under usual circumstances of use. Invokana can increase the risk of hypoglycemia when combined with insulin or a medication that increases insulin levels (e.g., a sulfonylurea). Therefore, a lower dose of insulin or insulin-raising medication may be required to minimize the risk of hypoglycemia when used in combination with Invokamet.

Janssen Pharmaceuticals, Inc. and its affiliates have rights to canagliflozin through a license agreement with Mitsubishi Tanabe Pharma Corporation. Janssen Pharmaceuticals, Inc. and its affiliates have marketing rights in North America, South America, Europe, the Middle East, Africa, Australia, New Zealand and parts of Asia.

On April 25, 2014, Janssen - Cilag International NV announced that the European Commission (EC) approved Vokanamet (a fixed-dose therapy combining canagliflozin and immediate release metformin hydrochloride in a single tablet) in the European Union, for the treatment of adults with type 2 diabetes mellitus to improve glycemic control. Invokana is approved as a single agent in Aruba, Australia, Brazil, Canada, Chile, Costa Rica, El Salvador, the European Union (31 countries), Guatemala, Kuwait, Mexico, Peru, Singapore, South Korea, Switzerland, United Arab Emirates, and the United States.

About Type 2 Diabetes

An estimated 371 million people worldwide are living with diabetes and approximately 29 million people have diabetes in the United States. Type 2 diabetes comprises 90 to 95 percent of people with diabetes, which is chronic and affects the body's ability to metabolize sugar (glucose), and is characterized by the inability of pancreatic beta cell function to keep up with the body's demand for insulin.
Nearly half of adults with type 2 diabetes do not achieve recommended levels of glucose control, and if left uncontrolled, type 2 diabetes can lead to serious complications. Improved glycemic control has been demonstrated to reduce the on set and progression of these complications.

About Janssen Pharmaceuticals, Inc.

As a member of the Janssen Pharmaceutical Companies of Johnson & Johnson, Janssen Pharmaceuticals, Inc. is dedicated to addressing and resolving the major unmet medical needs of our time. Driven by our commitment to patients, healthcare professionals, and caregivers, we strive to develop sustainable and integrated healthcare solutions by working in partnership with all stakeholders on the basis of trust and transparency. Our daily work is guided by meeting goals of excellence in quality, innovation, safety, and efficacy in order to advance patient care.

Sadifit - a hope for a healthy life?

Sadifit is an Ucranian product what contains natural vegetal products

Composition, structure and packing

collection filter bag 3 g, № 20

collection pack 75 g, int. package

Blueberry shoots 0.2 g / g
Common bean fruit pods 0.2 g / g
Green tea leaf 0.15 g / g
Peppermint leaves 0.05 g / g
Jerusalem artichoke (topinambour) tubers 0.2 g / g
Stevia leaves 0.2 g / g
№ UA/6114/01/01 from 19.03.2007 to 19.03.2012

Pharmacological action

Collection components contain inulin, amino acids, glycosides, tannins, vitamins, essential oils, flavonoids, saponins, organic acids, micro and macroelements. This complex of biologically active substances has hypoglycemic effect in type II diabetes mellitus with mild and moderate form, allowing in some cases, to reduce the daily dose of oral antidiabetic agents.
In addition, regulates the function of the gastrointestinal tract, stimulates the activity of the pancreas, normalizes metabolism, reduces cholesterol levels in the blood, has anti-inflammatory, choleretic and diuretic effects.

The dosage

6 g (1 tablespoon) of collection is placed in an enamel bowl, pour 300 ml (1.5 cups) of hot boiled water, cover with a lid and boil on water bath for 15 min. Cool it at room temperature for 45 minutes, filter, and squeeze the residue to the strained infusion.
To get the needed volume bring boiled water up to 300 ml. Adults take in warm form  1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on the age of 2 tablespoons up to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days. Before use, shake the infusion is recommended.

2 packet filter placed in a glass or enamel bowl, pour 300 ml (1.5 cups) of boiling water, cover and insist at least 1 hour Insisting recommended in a thermos. Adults take infusion in warm form  1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on age from 2 tablespoons to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days.

After a 7-10 days pause it is recommended to repeat the treatment.

Overdosage
reports of overdose have not been reported.

Drug Interactions
unknown.

Adverse effects
not identified.

Conditions and terms
Store in a dry, dark place. The prepared infusion - in a cool place (8-15 ° C) no more than 2 days.

Shelf life - 2 years.

Statement
light and medium forms of type II diabetes; gastrointestinal diseases (enterocolitis, chronic pancreatitis, chronic cholecystitis).

Contraindications
pregnancy; individual sensitivity to biologically active substances contained in the drug.

Cautions
take in warm form 30 minutes before eating.

Effect of Insulin on Fat Metabolism

Effect of Insulin on Fat Metabolism

Although not quite as visible as the acute effects of insulin on carbohydrate metabolism, insulin’s effects on fat metabolism are, in the long run, equally important. Especially dramatic is the long-term effect of insulin lack in causing extreme atherosclerosis, often leading to heart attacks, cerebral strokes, and other vascular accidents. But first, let us discuss the acute effects of insulin on fat metabolism.

Insulin Promotes Fat Synthesis and Storage

Insulin has several effects that lead to fat storage in adipose tissue. First, insulin increases the utilization of glucose by most of the body’s tissues, which automatically decreases the utilization of fat, thus functioning as a fat sparer.
However, insulin also promotes fatty acid synthesis. This is especially true when more carbohydrates are ingested than can be used for immediate energy, thus providing the substrate for fat synthesis.Almost all this synthesis occurs in the liver cells, and the fatty acids are then transported from the liver by way of the blood lipoproteins to the adipose cells to be stored.

 The different factors that lead to increased fatty acid synthesis in the liver include the following:

1. Insulin increases the transport of glucose into the liver cells.After the liver glycogen concentration reaches 5 to 6 per cent, this in itself inhibits further glycogen synthesis. Then all the additional glucose entering the liver cells becomes available to form fat. The glucose is first split to pyruvate in the glycolytic pathway, and the pyruvate subsequently is converted to acetyl coenzyme A (acetyl-CoA), the substrate from which fatty acids are synthesized.



2. An excess of citrate and isocitrate ions is formed by the citric acid cycle when excess amounts of glucose are being used for energy. These ions then have a direct effect in activating acetyl-CoA carboxylase, the enzyme required to carboxylate acetyl-CoA to form malonyl-CoA, the first stage of fatty acid synthesis.


3. Most of the fatty acids are then synthesized within the liver itself and used to form triglycerides,the usual form of storage fat. They are released from the liver cells to the blood in the lipoproteins.
   Insulin activates lipoprotein lipase in the capillary walls of the adipose tissue, which splits the triglycerides again into fatty acids, a requirement for them to be absorbed into the adipose cells, where they are again converted to triglycerides and stored.

Role of Insulin in Storage of Fat in the Adipose Cells.

 Insulin has two other essential effects that are required for fat storage in adipose cells:

1. Insulin inhibits the action of hormone-sensitive lipase. This is the enzyme that causes hydrolysis of
the triglycerides already stored in the fat cells.
Therefore, the release of fatty acids from the adipose tissue into the circulating blood is inhibited.

2. Insulin promotes glucose transport through the cell membrane into the fat cells in exactly the same
ways that it promotes glucose transport into muscle cells.
 Some of this glucose is then used to
synthesize minute amounts of fatty acids, but more important, it also forms large quantities of a-glycerol phosphate.
This substance supplies the glycerol that combines with fatty acids to form
the triglycerides that are the storage form of fat in adipose cells.
Therefore, when insulin is not available, even storage of the large amounts of fatty acids transported from the liver in the lipoproteins is almost blocked.
 
 References:
© Copyright Guyton and Hall Textbook of Medical Physiology

References:
© Copyright Guyton and Hall Textbook of Medical Physiology - See more at: http://how-to-get-rid-of-diabetes.blogspot.com/2014/07/insulin-promotes-glucose-metabolism.html#sthash.tKI5KMwU.dpuf

Physiopathology of endocrine pancreas. Insulin resistance

Insulin resistance
Type II diabetes is characterized by dysfunction of pancreatic beta cells and insulin resistance, in the majority of the tissues - peripheral target: skeletal muscle, liver, kidney, adipose tissue.

In insulin resistance ( in people with type II diabetes)  the dose of exogenous insulin increases significantly , which stimulate glucose uptake by tissues and inhibits endogenous glucose production.
Insulin resistance reflects the predominant defect in insulin action on skeletal muscles and liver.

The major causes of muscle insulin resistance in prediabetic stage are: genetic predisposition, obesity and physical hypoactivity.
Obesity and lack of exercise are major factors that contribute to the development of insulin resistance. It was established that exercise increases insulin sensitivity independent of body mass reduction and changes in body composition.
Thus, the children of parents with type II diabetes, physical training for 6 weeks increases glucose uptake and glycogen synthesis due to increased sensitivity to insulin.

Pharmacotherapy Principles of endocrine disorders

The basic principles of pharmacocorection is to restore hormonal homeostasis in the body through substitution treatment in endocrine hypofunction (thyroid hormone in hypothyroidism, estrogen or androgen administration in the hypogonadism, insulin in type I diabetes, etc.).
In case of endocrine gland hyperfunction it is necessary to administer preparations that inhibit gland function (eg Thyrostatic or radioactive iodine treatment - in hyperthyreosis).
Radical treatment involves surgical removal of hormonproductive tumors.

Physiopathology of endocrine pancreas. Insulin deficiency

Insulin deficiency

Insulin deficiency is the main cause of insulin-dependent diabetes pathogeny or type I diabetes.
Type I diabetes Mellitus is related to insulin deficiency consecutive to reduction of beta-pancreatic cells population. One of the major causes of diabetes Mellitus is inflammation with autoimmune alteration of Lagerhans islets (insulite). It has a specific and exclusive localisation in islets formed of beta cells, while in islets formed of glucagon producing cells inflammation is missing.

Insulin deficiency produces multiple metabolic disturbances with specific severe lesions of body structure.
Glycogen and lipid synthesis disturbances constitutes the basic and essential metabolic manifestation of insulin deficiency.
These are related with insulin/glucagon index.

The consequence of this thing is the impossibility of liver and muscles to synthesise glycogen and of adipocites to synthesise lipids from glucose.
Cardinal clinical signs of type I diabetes: reduced glucose tolerance, hyperglycaemia, protein catabolism intensification, hyperlipidemia, angiopathy and nephrotic syndrome.


The pathogenesis of hyperglycaemia is the fact that in the absence of insulin,  insulin-dependent glucose receptors in adipocytes and myocytes type IV reside in the cytoplasm,  are not exposed on the cell membrane, due to which the glucose can not be assimilated by the cells for synthesis of glycogen and fat.

The pathogenesis of hyperlipidemia (prevalent on account of the very low density lipoprotein and non-esterified fatty acids) can be explained by the fact that the lipase in the absence of adipocyte insulin remain phosphorylated, inactive, dietary fat are not incorporated into adipocytes, and unwanted fatty acids are converted in the liver to very low density lipoprotein.Increase blood concentration of non-esterified fatty acids (hyperlipidemia transport) is the consequence of intense mobilization of lipids from adipose tissue.

Hiperketonemia and ketonuria is due to high concentration of fatty acids in the blood with increased beta-oxidation and acetyl CoA abundant production, that in lack of insulin is not used for lipid resynthesis   but ketone bodies - acetone, hydroxybutyric acid and acetylacetic acid synthesis.

Renal syndrome in hypoinsulinism is constituted of  glucosuria due to hyperglycaemia and high glucose concentration in glomerular filtration, which exceeds the functional capacity of the  canalicular epithelium glucokinase (threshold is about 180 mg / dL).

Glucosuria leads polyuria (osmotic diuresis) and polydipsia. Development of diabetic nephropathy with microangiopathy leads to progressive decrease in glomerular filtration rate, with the growth of the permeability of renal filter and albuminuria.
Ketonuria is consecutive to hyperketonemia.

In the pathogenesis of diabetic angiopathy glycosylation of proteins - its IDDM process, which consists in the non-fermentative combination of glucose with amino acids amino-groups to form complexes of glucose and protein (ketone-amino-proteins​​) in the vessel wall .
Glycosylation changes the conformation of the protein molecule, the electric charge, alter the function of proteins, blocking the active center. Diabetic angiopathy is affecting both small vessels and large ones.

Diabetes can lead to coma - ketoacidotic in absolute insufficiency of insulin, hyperosmolar in moderate insulin deficiency and lactoacidotic in hypoxia, sepsis, cardiogenic shock. (An overdose of insulin can result in hypoglycemic coma).
Pathogenetic correction of homeostasis in ketoacidotic coma seeks liquidation of insulin deficiency, and  rehydration and resalinization of the body, restoring acid-base balance and glycogen reserves.

Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain

Lack of Effect of Insulin on Glucose Uptake
and Usage by the Brain

The brain is quite different from most other tissues of the body in that insulin has little effect on uptake or
use of glucose. Instead, the brain cells are permeable to glucose and can use glucose without the intermediation of insulin.

The brain cells are also quite different from most other cells of the body in that they normally use only
glucose for energy and can use other energy substrates, such as fats, only with difficulty.
Therefore, it is essential that the blood glucose level always be maintained above a critical level, which is one of the most important functions of the blood glucose control system.
When the blood glucose falls too low, into
the range of 20 to 50 mg/100 ml, symptoms of hypoglycemic shock develop, characterized by progressive
nervous irritability that leads to fainting, seizures, and even coma.

Effect of Insulin on Carbohydrate Metabolism
in Other Cells
Insulin increases glucose transport into and glucose usage by most other cells of the body (with the exception of the brain cells, as noted) in the same way that it affects glucose transport and usage in muscle cells.
The transport of glucose into adipose cells mainly provides substrate for the glycerol portion of the fat molecule.
 Therefore, in this indirect way, insulin promotes deposition of fat in these cells.
 
 References:
© Copyright Guyton and Hall Textbook of Medical Physiology