Me! I Disconnect From You

The answer to how bad junk food is for you depends on how much of it you eat.

According to the experts we consulted in making What's Really In Our Food?, having a burger or pizza now and again as part of a properly balanced diet that includes plenty of vitamins and nutrients is not going to damage your health.

Instead, most of the experts agreed that the real problem lies with what they call "junk diets". This is when people eat junk food to the exclusion of everything else.

Having a sugary breakfast, a burger for lunch and a pizza for dinner every day - and no fruit and vegetables - is the kind of diet that over the long term can lead to serious health problems including Type II diabetes, heart attack and stroke.

Almost one in five children under-15 are currently obese, and if current trends continue, more than half of the adult population could be clinically obese by 2050.

To help us make more informed decisions about what we eat dieticians sometimes refer to what are called "Guideline Daily Amounts" or GDAs for short.

These are daily targets to aim at in order that we do not eat the quantities of food that can lead to health problems.

Guideline daily amounts for men, women and children

Using this scale it is possible to assess how some types of fast foods can contribute a huge number of calories, salt, fat or sugar in a single portion.

For example, a Burger King double whopper with cheese contains 923 calories. That is almost half what a woman should eat in an entire day.

A muffin from a high street coffee chain can contain 500 calories. This is a fifth of a man's guideline daily amount in one snack.

Equally a single slice of Domino's double decadence cheese and tomato pizza can contain 1.9g of salt, or about a third of the guideline daily amount for both men and women.

With this in mind, the recommendations of the experts we talked to was that we should view junk food as a treat and not a staple.

We should be careful about not eating it too much or too often and try to eat small portions.

And we should also try to eat lots of fruit and vegetables. This is something many fast food companies have already taken on board and are trying to offer a greater range of products.

So if you love junk food - do not worry - you do not have to give it up.

What's Really In Our Food? was broadcast from Monday 26 to Friday 30 November 2007 at 0915 GMT on BBC One.


This is a part of article Do I need to give up junk food? Taken from "Generic Amaryl (Glimepiride) Information" Information Blog

Labels: pharmacology

Acarbose Improves Glycemic Control in Overweight Type 2 Diabetic

from Diabetes Care

Results

A total of 83 patients were randomized to the two treatment arms. Of those, 2 patients were excluded from the ITT analysis for HbA1c (acarbose n = 38, placebo n = 43) and 1 patient had no baseline fasting blood glucose data and was thus excluded from the ITT analysis for FBG (acarbose n = 39, placebo n = 43). In the PP population, 71 patients were included for HbA1c analysis (acarbose n = 33, placebo n = 38) and 74 for FBG analysis (acarbose n = 35, placebo n = 39). All randomized patients were included in the safety analysis (acarbose n = 40, placebo n = 43). Baseline demographic data and efficacy variables of all randomized subjects compared well between the treatment groups (Table 1). Both treatment groups received the same median dosage of metformin (1,700 mg/day).

Figure 1A shows the change in mean HbA1c levels during the study course (ITT analysis). Significant differences between the treatment groups compared to baseline were seen for weeks 12 and 24 (P = 0.0009 and P = 0.0023, respectively). Mean HbA1c levels increased in the placebo group from 7.82 ± 0.83% at baseline to 8.1 ± 1.06% at week 12 and 8.5 ± 1.44% at study end. The mean increase after 24 weeks was 0.68 ± 1.17%, with a significant overall time effect (P = 0.0001). In the acarbose group, levels decreased from 8.02 ± 0.85% at baseline to 7.78 ± 1.0% at week 12 (P = 0.0261). Levels then increased to 7.97 ± 1.1% at study end (mean change after 24 weeks was -0.05 ± 0.8%). There was no significant overall time effect for acarbose. The adjusted least square means for the change in HbA1c from baseline to week 24 showed a reduction of 0.16 ± 0.18% in the acarbose arm compared to an increase of 0.86 ± 0.16% in the placebo group, with a statistically significant difference between the treatment arms of 1.02% (95% CI 0.543-1.497, P = 0.0001). There was a significantly greater proportion of responders in the acarbose group (n = 18; 47%) than in the placebo group (n = 6; 14%) (P = 0.001) at the end of the study.

Figure 1. (click image to zoom) Change in mean HbA1c (A) and mean FBG (B) during a 24-week treatment period with acarbose (•) or placebo () adjunctive therapy in the ITT population.

Mean levels of the secondary efficacy variable FBG increased in the placebo arm from baseline (9.41 ± 1.99 mmol/l) to week 4 (10.06 ± 2.43 mmol/l) and continued to increase to the end of study (10.77 ± 3.39 mmol/l), whereas levels in the acarbose arm varied only slightly from baseline (Fig. 1B). The mean increase was 1.36 ± 2.88 mmol/l for the placebo and 0.08 ± 1.98 mmol/l for the acarbose group. The adjusted least square means showed an increase at end point in both groups: 0.34 ± 0.42 mmol/l for acarbose compared to 1.48 ± 0.39 mmol/l for placebo patients, with a statistically significant difference of 1.132 mmol/l between the two groups (95% CI 0.056-2.208, P = 0.0395). PP analyses for both variables showed similar results, but were not statistically significant for treatment differences concerning FBG.

Of the 83 patients valid for safety analysis, 76 completed the study. Mean study duration was 169 days for both acarbose (29-184 days) and placebo (39-176 days). Overall compliance (80-120% compliance) was 100% for acarbose and 95.3% for placebo patients. In all, five patients reduced the medication dose to 50 mg b.i.d. because of adverse events (acarbose, n = 3; placebo, n = 2); three of these patients later reverted back to the original dosage. Patients in both treatment groups experienced a small mean weight reduction over the study period (1.32 ± 2.37 kg for acarbose vs. 0.43 ± 2.9 kg for placebo patients), which was not significantly different (P = 0.13). There were also no significant changes in vital signs. Changes in routine laboratory parameters were similar in both treatment groups, except for one patient (acarbose group) with elevated liver function enzymes who was withdrawn from the study. In total, seven patients were prematurely withdrawn from the study during the 24-week treatment period: four because of treatment-emergent adverse events, one patient on placebo because of constipation and depression, and three patients on acarbose with flatulence, flatulence accompanied by abdominal pain, and the aforementioned elevated liver enzymes. A serious adverse event with remote or no relation to the study medication was experienced by two acarbose patients and one placebo patient; no fatalities occurred. Treatment-emergent adverse events with a relation to the study medication rated as "possible" or "probable" were reported by 75% of acarbose and 55.8% of placebo patients. The main difference between the treatment groups was the higher frequency of gastrointestinal complaints in the acarbose group (Table 2).

This is a part of article Acarbose Improves Glycemic Control in Overweight Type 2 Diabetic Taken from "Generic Amaryl (Glimepiride) Information" Information Blog

Labels: pharmacology

Viagra - it is the drug that has transformed the lives of millions and changed the way we think about sex forever.

The rise and rise of Viagra has created a £1.5bn worldwide market in anti-impotence pills.

Now rivals are fighting for a share of the spoils and it is becoming a recreational drug of choice for some in the party generation.

Last week, Pfizer's chief executive Henry McKinnell warned that Chinese made counterfeits posed a threat to its business and urged the country's authorities to clamp down on the copycats.

New research

Pfizer, the world's biggest pharmaceutical company, stumbled on the drug by accident at their research labs in Sandwich, Kent.

In the late 1980s, they had been developing a new treatment for angina, but noticed a strange side-effect in trials - increased erections among volunteers.

The effect on their sex lives was so marked that once the angina trails were over the volunteers wanted to keep on taking the medication.

Pfizer decided to commission some new research.

In 1989 they approached Clive Gingell, one of Britain's top Urological Surgeons, based in Bristol.

He had spent his whole career trying to treat and improve the lives of thousands of men suffering from impotence.

In those days, commonly used treatments included the fitting of implants directly into the penis, a vacuum pump and self injection.

Most sufferers were thoroughly put off and consigned themselves to a life without sex.

Viagra arrives

Mr Gingell ran a new series of trials, and the results impressed him.

He describes Viagra as "a wonder drug".

"The thought of having a pill that would cure impotence was amazing to me," he says.

"I never thought I would see it in my lifetime."

"There has been a kind of Holy Grail idea associated with curing impotence," Pfizer's Mariann Caprino tells the Money Programme.

"And here it was in a little blue pill."

Colossal market

When Viagra was launched in 1998, Pfizer's share price doubled. It was apparent that there was a huge previously untapped market out there.

Doctors claim that half of all men over 40 become impotent at some point in their lives.

That is more than 150 million worldwide, with two million sufferers in Britain alone, so the potential market for drugs like Viagra is colossal.

Overnight Viagra made Pfizer famous. "We discovered the mass production of penicillin, yet it was Viagra that put Pfizer on the map," says Ms Caprino.

Embarrassing subject

Nevertheless, despite the highly successful launch, the company faced a huge potential problem in selling Viagra.

Men were simply not willing to talk about impotence, they were ashamed.

If they were not prepared to discuss their impotence, how could they be persuaded to ask their doctor for a prescription?

Ray Reynolds, who suffered from impotence for 30 years, had simply given up hope of ever being able to have sex again.

"I thought well, I'll just put it to one side and remain a eunuch for the rest of my life," he says.

Celebrity endorsement

To overcome the problem, Pfizer came up with a series of marketing ploys.

Firstly, they asked the Vatican, and other world religious leaders, for their blessing. This headed off possible moral and religious objections.

Secondly, they employed big name celebrities to encourage men to seek treatment for impotence.

Pele, the legendary footballer, headed a men's health campaign about erection problems, and 75 year old former US Presidential candidate Bob Dole went public for Pfizer about his own impotence problem.

American men rushed to their doctors.

Leon Steinberg, an 84-year-old impotence sufferer living in a retirement community in Florida, was impressed by Mr Dole's courage in coming forward.

"When I saw it on TV, I admired him for it," he says.

"You might say he was my idol."

Withdrawal of campaign

Pfizer decided not to use the term "impotence" in the advertisements, instead replacing it with a more bland technical term "erectile dysfunction".

Pfizer's Mike Suesserman says the new term "allowed us to make the condition a household name".

Pfizer reasoned that few men may admit to impotence, which employs a complete loss of ability, but a lot more may own up to erectile dysfunction, which suggests a much broader range of symptoms.

But Pfizer's aggressive marketing campaign has recently run into trouble.

A recent television advertisement has been criticized in the United States for suggesting that Viagra might be better and more effective for patients than the clinical experience suggests.

The Food and Drug Administration ordered its withdrawal.

Efficient sex

There are potential problems, too, in the increasing use of Viagra as a recreational drug.

"For a lot of gay people it is just a normal way of life," says Gary Mercado, who runs the Elysium Resort, the largest gay hotel in Fort Lauderdale, Florida.

When Viagra is taken with amphetamines, "you forget about having protective sex, so there are huge capabilities of transmitting all sorts of sexual diseases", he says.

Pfizer says that a very small percentage of people abuse Viagra, but accepts there is great potential in developing the market for sexual pharmaceuticals.

Meika Loe, author of the book The Rise of Viagra, agrees: "In the Viagra era, sexuality is subject to the cult of efficiency. It's become almost McDonald's-ised. Serve it up fast and hot."

The Money Programme: Viagra: The Hard Sell was broadcast at 2200 GMT on Wednesday, 9 February on BBC Two .
This is a part of article Viagra: the hard sell Taken from "Erectile Disfunction Medication" Information Blog

Labels: pharmacology

In This Journal ScanPediatric ResearchChestCirculation ResearchThe New England Journal of Medicine

Pulmonary Hypertension, February 2006 Journal Scan

FromChestFebruary 2006  ( Volume 129, Number 2 )

Pulmonary Hemodynamic Responses to Brain Natriuretic Peptide and Sildenafil in Patients With Pulmonary Arterial HypertensionKlinger JR, Thaker S, Houtchens J, Preston IR, Hill NS, Farber HW 
Chest.  2006;129(2):417-425

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are proteins that are expressed in the heart.[1] These peptides raise the intracellular cyclic guanosine monophosphate (cGMP) levels to cause vasorelaxation. Another benefit of these peptides is the inhibition of vascular smooth muscle proliferation.[2] Study results have demonstrated inhibition of pulmonary vasoconstriction in pulmonary arterial rings by these 2 peptides[3] and the development of increased pulmonary artery pressures when the gene for encoding of ANP is disrupted.[4] The exact hemodynamic response to these peptides in patients with pulmonary arterial hypertension (PAH) has not been adequately studied, but the use of natriuretic peptides in patients with left heart disease and chronic hypoxic lung disease has demonstrated a decrease in pulmonary artery pressure (PAP).

This study looks at the effect of BNP acutely on hemodynamics (compared with inhaled nitric oxide [iNO] and epoprostenol) in patients with PAH and then the effect on hemodynamics when the pohsphodiesterase-5 (PDE-5) inhibitor sildenafil is added. This open-label study ran from September 2002 to June 2003 and enrolled 13 patients. Inclusion criteria included mean PAP (mPAP) levels > 25 mm Hg at rest, and a World Health Organization class I PAH group. They also had to be de novo patients. All patients had a Swan-Ganz catheter placed and received epoprostenol and, in addition, 8 patients also received iNO. They then received 2 infusions of the human B-type natriuretic peptide nesiritide. The second infusion of nesiritide occurred 1 hour after a single dose of oral sildenafil.

Hemodynamics were evaluated at various points during each separate drug administration. Plasma BNP levels were also obtained. mPAP was 48.6 ± 3.7 mm Hg and mean pulmonary vascular resistance (PVR) was 698 ± 105 dynes·cm/s². The resultant findings were decreased mPAP with both iNO and epoprostenol and an increase in cardiac index and decrease in PVR with epoprostenol. The BNP infusion on its own did not affect mPAP or PVR. With 1 dose of sildenafil, the mPAP and PVR did drop below baseline, and the addition of BNP after the sildenafil dose resulted in a further decline in mPAP. The decrease in mPAP and PVR in this group remained visible for up to 6 hours after stopping the BNP infusion, signifying the longest duration of response of all the groups. Only 1 patient demonstrated a vasodilator response to epoprostenol or sildenafil alone, but 4 of 12 patients demonstrated a positive vasodilator response to sildenafil with BNP.

Increased circulating BNP levels may help slow right ventricular remodeling and may even inhibit the proliferation of pulmonary vascular smooth muscle. With their effect on endothelin synthesis (inhibition), the natriuretic peptides could improve the effects of endothelin receptor antagonists. What is uncertain here is the rationale for the lack of response (decreased mPAP and PVR) to the BNP infusion alone but the positive response when sildenafil was added. The authors believe that the dose or duration of the BNP infusion may not have been adequate. Further studies are needed to determine whether there is a place for chronic BNP therapy in the treatment of PAH.ReferencesHill NS, Klinger JR, Warburton RR, et al. Brain natriuretic peptide: possible role in the modulation of hypoxic pulmonary hypertension. Am J Physiol. 1994;266:L308-L315.Hutchison HG, Trindade PT, Cunanan DB, et al. Mechanisms of natriuretic-peptide-induced growth inhibition of vascular smooth muscle cells. Cardiovasc Res. 1997;35:158-167.Klinger JR, Warburton RR, Pietras L, et al. Brain natriuretic peptide attenuates the development of pulmonary hypertension in hypoxia-adapted rats. J Appl Physiol. 1998;84:1646-1652.Klinger JR, Warburton RR, Pietras L, et al. Genetic disruption of atrial natriuretic peptide causes pulmonary hypertension in normoxic and hypoxic mice. Am J Physiol. 1999;276:L868-L874.

Abstract

This is a part of article Pulmonary Hypertension, February 2006 Taken from "Erectile Disfunction Medication" Information Blog

Labels: pharmacology

In This Journal ScanThe New England Journal of MedicineThoraxChestAmerican Journal of Respiratory and Critical Care Medicine

Pulmonary Medicine, October 2005 Journal Scan

FromThoraxOctober 2005  ( Volume 60, Number 10 )

Pepsin Like Activity in Bronchoalveolar Lavage Fluid Is Suggestive of Gastric Aspiration in Lung AllograftsWard C, Forrest IA, Brownlee IA, et al 
Thorax.  2005;60(10):872-874

Bronchiolitis obliterans (BO), the pathologic correlate of chronic allograft rejection, is the entity that is the most common cause of a patient's demise beyond the first post-lung transplant year. This remains 1 of the major reasons why outcomes after lung transplantation continue to lag behind that of other solid organ transplants. As yet, there are no proven effective therapies for BO. Any intervention that might reduce the incidence of BO might have a significant impact on survival. Similarly, early identification of treatable risk factors could have significant long-term benefits. One such risk factor appears to be chronic aspiration. For a number of reasons lung transplant recipients might be at higher risk for aspiration. Specifically, vagal innervation might be disrupted as a result of the surgery and the calcineurin inhibitors are known to reduce gastric motility. Most of the work highlighting the potential association of BO with gastroesophageal reflux disease has come from the group at Duke.[1-4] It is therefore gratifying that another group has produced data consistent with that of the Duke groups, which lends further credence to the association.

In this article, from the British group at Newcastle upon Tyne, the authors looked at levels of pepsin in the bronchoalveolar lavage samples of 13 lung transplant recipients. These patients were 3-87 months out from their transplants. All of them were on standard triple immunotherapy, 10 were taking prophylactic proton pump inhibitors, and all were free from any symptoms suggestive of gastroesophageal reflux disease. They compared the pepsin levels of these patients to those of 4 normal nonsmoking controls (who they somehow talked into undergoing bronchoscopy!). These controls were invaluable as they underscore the importance of the results found in the patients, specifically the levels of pepsin in the controls were < 1 ng/mL vs 109 ng/mL in the patients (range, 35-1375). Small numbers perhaps, big difference definitely, and a P value of .003 to underscore this.

The scary implication of this study is that all lung transplant recipients aspirate and can remain symptom-free, acid-free, and still potentially suffer the deleterious consequences of proteolytic activity in the lungs. This study raises a number of questions. First, is it possible that enzymatic activity precipitates an exaggerated or ongoing immune response? Could it be that BO is not an immunologic injury after all? What is needed to validate these findings is a study showing a correlation between bronchoalveolar lavage pepsin levels and the subsequent development of BO. A retrospective study showing that fundoplication halts or reverses BO has already been performed by the group at Duke[4]. .. food for thought indeed!ReferencesDavis RD, Lau CL, Eubanks S, et al. Improved lung allograft function after fundoplication in patients with gastroesophageal reflux undergoing lung transplantation. J Thorac Cardiovasc Surg. 2003;125:533-542.Lau CL, Paler SM, Howell DN, et al. Laparoscopic antireflux surgery in the lung transplant population. Surg Endosc. 2002;16:1674-1678.O'Halloran EK, Reynolds JD, Lau CL, et al. Laparoscopic Nissen Fundoplication for treating reflux in lung transplant recipients. J Gastrointest Surg. 2004;8:132-137.Cantu E, Appel JZ, Hartwig MG, et al. Early fundoplication prevents chronic allograft dysfunction in patients with gastroesophageal reflux disease. Ann Thor Surg. 2004;78:1142-1151.

Abstract

This is a part of article Pulmonary Medicine, October 2005 Taken from "Erectile Disfunction Medication" Information Blog

Labels: pharmacology

Conclusions

The results of the IMHS constitute a valuable contribution to the literature on real-world data on users of sildenafil. Instead of evaluating CVD events in men enrolled in clinical trials, the IMHS included men in the general population who were prescribed sildenafil. The results are consistent with previous analyses, suggesting that the incidence of CVD events in men prescribed sildenafil for ED was low and similar to those in clinical trials and the UK PEM study. The results also support previous reports that ED and CVD share risk factors and that men with ED are at greater risk for CVD events than those without ED.

CLICK HERE for subscription information about this journal.  Printer- Friendly Email ThisFunding Information

The study was sponsored by Pfizer Inc. Murray A. Mittleman has served as a consultant to Pfizer Inc., Lily ICOS LLC and Bayer Healthcare, and has previously received research funding from Pfizer Inc. Statistical support was provided by Xiaofeng Zhou of Pfizer Inc. Editorial support was provided by Carl Clay, PhD, and Deborah M. Campoli-Richards, BSPHA, RPh, at Complete Healthcare Communications, Inc., and was funded by Pfizer Inc.Reprint Address

Dr Murray A. Mittleman, Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave - MASCO 423, Boston, MA 02215, USA, Tel.: + 617 632 7694, Fax: + 617 632 7698, Email: mailto:mmittlem@hsph.harvard.edu

Int J Clin Pract.  2008;62(3):367-373.  ©2008 Blackwell Publishing
This is a part of article Cardiovascular Outcomes Among Sildenafil Users Taken from "Erectile Disfunction Medication" Information Blog

Labels: pharmacology

Diabetes Today

from Drug Benefit Trends

What's Ahead

While the ADA and other organizations fight — unsuccessfully, for now — for additional federal funding for research, studies of ways to stop or slow the devastating effects of diabetes continue. The AAHP and the ADA have joined forces in a national effort, "Taking on Diabetes." The goal is to promote successful diabetes care by advancing effective clinical practices, developing worksite health programs and community partnerships, and providing annual education programs. As of May, 335 health plans had pledged to participate. Diabetes programs are slowly shifting from targeting only the sickest patients — or those having the most difficulty managing the disease — to more comprehensive efforts that provide additional care and support to every patient with diabetes within a particular health plan, employer group, or community.

Section 6 of 6
Drug Benefit Trends 11(11sb):5-10, 1999. © 1999 Cliggott Publishing, Division of SCP Communications
This is a part of article Diabetes Today Taken from "Generic Amaryl (Glimepiride) Information" Information Blog

Labels: pharmacology

Last report: most of visitors prefer free nude movies videos, not freeshemalemovies pics.

Labels: Annonce

Conception and Text editionConstruct

Goal: Liraglutide is a long-acting glucagon-like peptide 1 analog designed for once daily intromission.
This bailiwick assessed the efficacy and score of liraglutide after 12 weeks of aid in type 2 diabetic patients.
Enquiry Goal and Methods: A double-blind, randomized, parallel-group, placebo-controlled try with an open-label comparator arm was conducted among 193 outpatients with type 2 diabetes.
The mean age was 56.6 long time and the mean HbA1c was 7.6% across the idiom groups.
Patients were randomly assigned to one of five fixed-dosage groups of liraglutide (0.045, 0.225, 0.45, 0.60, or 0.75 mg), vesper, or open-label sulfonylurea (glimepiride, 1-4 mg).
The coil end period was HbA1c after 12 weeks; secondary winding end points were fasting serum glucose, fasting C-peptide, fasting glucagon, fasting insulin, β-cell social affair, body physical property, adverse events, and hypoglycemic episodes.
Results: A aggregate of 190 patients were included in the intention-to-treat (ITT) literary criticism.
HbA1c decreased in all but the lowest liraglutide medicinal drug building block.
In the 0.75-mg liraglutide building block, HbA1c decreased by 0.75 percent points (P < 0.0001) and fasting glucose decreased by 1.8 mmol/l (P = 0.0003) compared with medicinal drug.
Transmutation in glycemic bodily function was evident after 1 week.
Body weighting decreased by 1.2 kg in the 0.45-mg liraglutide grouping (P = 0.0184) compared with medicinal drug.
The proinsulin-to-insulin quantitative relation decreased in the 0.75-mg liraglutide abstract entity (-0.18; P = 0.0244) compared with medication.
Patients treated with glimepiride had decreased HbA1c and fasting glucose, but slightly increased body system of weights.
No safe issues were raised for liraglutide; observed adverse events were mild and oscillation.
Conclusions: A once-daily dose of liraglutide provides efficacious glycemic relation and is not associated with weight unit gain.
Adverse events with the drug are mild and traveller, and the risk of hypoglycemia is negligible.Institution

Type 2 diabetes is characterized by insulin resistor and defective β-cell computer software and is associated with hyperglucagonemia, increased hepatic glucose display, and obesity. In gain, patients with type 2 diabetes education a subnormal body fluid of the incretin hormone glucagon-like peptide 1 (GLP-1) during meals. Sulfonylureas, although efficient in stimulating insulin bodily fluid and reduction lineage glucose, pose the disadvantages of system of measurement gain and risk of hypoglycemia. Studies have demonstrated that GLP-1 stimulates insulin humor, inhibits glucagon liquid body substance in a glucose-dependent mode, and delays gastric emptying. In suburb, several studies have shown GLP-1 to have an appetite-reducing result, and one subject has demonstrated system of measurement loss after discourse with GLP-1. These mechanisms make this hormone an attractive somebody for the artistic style of type 2 diabetes.
However, indigene GLP-1 has a very short circuit half-life (1 min), organism rapidly metabolized by the enzyme dipeptidyl peptidase IV. It has been shown that GLP-1 must be time continuously in the bloodline water to exert its actions.

Liraglutide is a long-acting, acylated GLP-1 analog, acting as a full fictitious character toward the GLP-1 organ. Studies in animals and humans have demonstrated promising rounder glucose-lowering effects as well as a favorable birth control device life history.
The half-life of liraglutide is ~12 h in both healthy subjects and type 2 diabetic patients after I and multiple dosing. The dosing regimen is a once daily shot.
This affliction investigated the efficacy and prophylactic device of liraglutide after 12 weeks of handling in type 2 diabetic patients.

This is a part of article Improved Glycemic Control With No Weight Increase in Patients With Type 2 Diabetes After Once-Daily Treatment With the Long-Acting Glucagon-Like Peptide 1 Analog Liraglutide (NN2211) Taken from "Generic Amaryl (Glimepiride) Information" Information Blog

Labels: pharmacology