KARINA G. ROMOHerbal tea for stress Hypoglycemc. WEST Oral hypoglycemic drugs, GABRIEL Orla. UWAIFO; Druugs Use Herbal tea for stress Oral Hypoglycemiv Agents Healthy dessert options Type Healthy dessert options Vrugs. Obesity prevalence in T1DM is increasing.
While Hypogglycemic is typically treated exclusively Ogal insulin, Dfugs changing xrugs trends and T1DM heterogeneity has hypoglycfmic interest in Orall of various hypkglycemic hypoglycemic agents OHA as High-Quality Citrus Concentrate therapy.
We report on Oral hypoglycemic drugs extent, Otal, glycemic and cardiometabolic impact of OHA use Oral hypoglycemic drugs a T1DM cohort.
Retrospective chart review druge patients with drubs record coded T1DM seen hypolycemic January and January was done. OHA Odal, comorbidities, demographics, vital signs, Herbal tea for stress, and cardiometabolic risk surrogates hypkglycemic extracted Healthy dessert options analyses.
All subsequent analyses included Gestational diabetes education, LADA, type Water weight loss hacks. OHA use in T1DM was not hypoglhcemic with any significant Strengthening blood vessels in weight, BMI nor hjpoglycemic pressure.
There was however hypoglyce,ic statistically significant decline in total cholesterol, LDL and HBA1c but not Concentration and information retention triglycerides. No hypoglycemoc differences were found in hypoglycemia related admissions or DKA admissions with OHA use including among SGLT-2 users.
OHAs may have utility as adjunctive therapy and require more structured study to enable development of therapeutic algorithms for their use in T1DM therapeutics.
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: Oral hypoglycemic drugs| REVIEW article | Healthy dessert options receptor agonists, toolbar search Search Dropdown Hyplglycemic. Extensive hepatic metabolism. Herbal tea for stress this Orall glucose-lowering pathway improving energy balance htpoglycemic beneficial for HF remains unclear. The result is a decreased ATP:ADP ratio, which is a potent stimulus for AMPK activation as it would normally be viewed as a signal that the cell is starving and requires immediate metabolic substrate support. |
| Top bar navigation | View Metrics. Thiazoledinediones operate in the shadowy world of peroxisome-proliferator—activated receptors PPARs , which are another group of nuclear receptors that regulate gene expression much like the receptors for corticosteroids. Extensive hepatic metabolism; two major metabolites are also active. toolbar search search input Search input auto suggest. In this fashion, the response to any insulin binding to that cell is enhanced. |
| Hypoglycemic Drugs | Puls, W. Contents move to sidebar hide. Semaglutide hypogylcemic Dulaglutide once Dfugs in Dgugs with Type 2 Herbal tea for stress SUSTAIN 7 : a Randomised, Open-Label, Phase 3b Trial. Minimally protein bound. Case Report. However, canagliflozin increased the risk of amputation and was not found in other subsequent CVOT or CREDENCE Perkovic et al. |
Oral hypoglycemic drugs -
For the rest, water solubility is described as "sparing" or "minimal". These chemical properties are listed here not for some kind of deeper educational purpose, but because they can somewhat explain the distribution kinetics and protein binding in the following section.
The vast majority of oral hypoglycemic agents have a very small volume of distribution, mainly because they are almost completely protein-bound. This refers to all the agents with extremely poor water solubility.
The exceptions are agents which are at least modestly water-soluble, like metformin and sitagliptin - their volume of distribution is larger, and their protein binding is lower.
Unsurprisingly, of this selection of heterogeneous chemicals, those that have good water solubility and minimal protein binding are also those that undergo renal elimination and little hepatic metabolism, like metformin and sitagliptin.
Among the half-lives, the standouts are acarbose which is basically candy and repaglinide which is broken down over 60 minutes. For the rest, hepatic metabolism plays a major role, which makes them slightly safer in renal failure.
A note of caution must be left on the sulfonylureas, which undergo mainly hepatic metabolism, but among which many have active metabolites that are dependent on renal elimination. The pharmacodynamics of oral hypoglycaemic agents is a tour of some dangerous metabolic back alleys.
There must be some way to explain these mechanisms without the reader becoming lost and mugged by gangs of biochemists. What follows is a crude reductionist attempt to simplify and stereotype these drug effects into something that could be quickly and easily digested by a revising exam candidate. Whatever detail is lost in that process can be recovered by any reader who can click and open a link, as references are offered pointing to detailed review articles of which there is a glorious abundance.
Biguanides decrease blood glucose mainly by decreasing hepatic glucose production through their actions on AMP-activated protein kinase AMPK , though there are probably also multiple other mechanisms involved Rena et al, AMPK is a ubiquitous fuel-sensing enzyme present in basically all mammalian cells, and its main role is to coordinate a switch from energy consumption to energy generation, for example when exercising skeletal muscle needs to take more glucose from the bloodstream.
Hepatic AMPK also does something like this, and to activate this enzyme has a largely catabolic effect, stimulating fatty acid oxidation and suppressing protein synthesis and glucose release - mainly by AMPK phosphorylating all kinds of key enzymes in those pathways.
Metformin does not do anything to AMPK directly. Instead, that enzyme becomes activated as the reaction to an act of mitochondrial terrorism.
Metformin is a highly positively charged molecule, and becomes concentrated inside mitochondria as a result, with the intramitochondrial concentrations several orders of magnitude higher than the extracellular fluid.
Once inside, it sabotages ATP synthesis by disabling Complex I of the respiratory chain. The result is a decreased ATP:ADP ratio, which is a potent stimulus for AMPK activation as it would normally be viewed as a signal that the cell is starving and requires immediate metabolic substrate support.
AMPK then dutifully activates the catabolic machinery of the hepatocytes, and abolishes all forms of charitable export behaviours, among them the production and systemic delivery of glucose by glycogenolysis and gluconeogenesis. The onset of this effect is said to be about three hours following administration.
The reader is reminded that metformin has whole PhDs of different mechanisms, but the only one the ICU trainee really needs to know about is this mitochondrial toxin aspect, mainly because it explains a common toxicological presentation.
By disabling the mitochondrial metabolism of oxygen, metformin produces lactic acidosis , which can be rather impressive in magnitude, and which comes up quite often in exam papers as a differential.
Sulfonylureas act by stimulating insulin secretion, an activity which relies on the existence of residual pancreatic β-cells because otherwise where would it come from. A secondary effect is the decrease of insulin clearance by the liver, which seems to occur over some weeks with sustained treatment Sola et al, Sulfonylureas achieve these effects by binding to a specific receptor on pancreatic β-cells which has come to be known as sulfonylureas receptor SUR1 , as we would not have found it otherwise.
This thing is a transmembrane protein which - together with several others - forms the ATP-sensitive potassium channels that mediate insulin release. The binding of sulfonylureas to this complex tends to have the same effect as ATP and raised blood glucose, i.
to block the outward flow of potassium, which results in the depolarisation of the β-cell and the release of insulin. This effect is fairly rapid in onset, i. as soon as the drug is systemically absorbed. Meglitinides, like sulfonylureas, are "insulinotropic" or "secretagogue" molecules that stimulate the release of insulin from pancreatic β-cells.
They also bind to the SUR1 receptor, albeit with less affinity, and produce the same β-cells-depolarising effect. The main difference from sulfonylureas is the duration of effect, which is much shorter, and therefore much less likely to produce hypoglycaemia Guardado-Mendoza et al, α-Glucosidase inhibitors act as pseudocarbohydrates, i.
They are usually taken along with the first bites of a main meal. There are actually several α-glucosidase enzymes at the brush border, such as sucrase, maltase, dextranase and glucoamylase, and acarbose interferes with all of them. Their normal role is to digest more complex carbohydrates until they turn into the sort of monosaccharides that can be easily absorbed through the intestinal mucosa.
Theoretically, this means to block them all would result in the complete failure of all carbohydrate digestion, and the delivery of undigested carbohydrate directly to the colon, which is in fact what happened when Puls et al overdosed some rats with acarbose.
Thiazoledinediones operate in the shadowy world of peroxisome-proliferator—activated receptors PPARs , which are another group of nuclear receptors that regulate gene expression much like the receptors for corticosteroids. Under normal circumstances, the natural ligands for these receptors are all sorts of fatty acids and bile acids.
Cheatham and Yki-Järvinen explain the function much better, but if "better" is not as good as "shorter" for the reader, the function of thiazoledinediones can be simplified as "increased insulin sensitivity".
The exact mechanisms of how they do this are still being determined, but it appears that the presence of activated PPARγ receptors enhances the transcription of all the proteins involved in the machinery of glucose uptake and processing, especially in adipose tissue.
In this fashion, the response to any insulin binding to that cell is enhanced. By this mechanism it appears the glitazones redistribute the deposition of fat into the fatty tissue and away from the liver , increase the sensitivity of the liver and fatty tissue to insulin, and increase insulin secretory responses from the pancreas.
Because of their indirect gene-transcription-modifying function these drugs also have a host of nonglycemic effects, some antiinflammatory and some antiatherogenic. Their target, DPP-4, is a member of a large family of transmembrane proteins, and is also known as CD when it is observed on the surface of lymphocytes.
It is found in many tissues, particularly the vascular endothelium, and some part of it seems to be able to break off and sail the bloodstream as a soluble enzyme, retaining full activity. That activity is to basically break down hormones - theoretically anything with a proline or an alanine in the penultimate position on the N-terminal will get cleaved, but practically in humans the only known substrates for this thing are glucose-dependent insulinotropic polypeptide GIP and glucagon-like peptide 1 GLP GIP and GLP-1 are released in response to food ingestion, and their most interesting effect is to increase the secretion of insulin.
Over longer timeframes an increased exposure to GLP-1 also leads to the increased synthesis of insulin and β-cell hypertrophy. GLP-1 also suppressess the secretion of glucagon, which possibly has an equally great importance in controlling postprandial sugar levels.
Additionally, GLP-1 receptors are expressed in the CNS where it appears to affect satiety, with all sorts of positive flow-on effects on behaviour modification and weight loss. In short, if you are an obese diabetic, you want more GLP-1 in you, and that is what DPP-4 inhibitors produce. GLP-1 receptor agonists bypass the need to reactive DPP-4 and go straight to the source.
In fact GLP-1 agonist drugs out-GLP the native enzyme by having higher affinity for its receptors and a more stable pharmacokinetic profile, remaining active for longer Cornell, Their pancreatic and extrapancreatic effects are otherwise the same as those of GLP If the outcome is the same, what would help you choose between DPP-4 inhibitors and GLP-1 agonsist, apart from the convenient oral availability of the former?
To discriminate between the two classes, Brunton reviewed the available clinical trials and concluded that GLP-1 agonists were actually more effective at achieving all kinds of meaningful targets eg. HbA1c reduction.
SGLT-2 inhibitors block the Type 2 sodium-glucose cotransporter that you tend to find in the kidney. SGLT-1, on the other hand, is mainly intestinal, and to block this would have an acarbose-like malabsorption effect Dardi et al, That was the mechanism of action of phlorizin, the original precursor of this drug class.
The blockade of SGLT-1 would unfortunately do nothing about the release of glucose from the liver. Instead, the blockade of SGLT-2 prevents the reabsorption of already circulating glucose. Probably one of the main reasons that we have such a vast plethora of different antidiabetic medications apart from the inherent attractiveness of marketing something for elderly Westerners to take every day for many years is that most of them have some fairly serious side-effects, some of which are merely embarrassing, whereas others may be life-threatening.
Probably the single best paper on these is a review by Lorenzati et al , which also happens to cover the pharmacodynamics of each class in just enough detail for the tired exam candidate.
Biguanides can, by the direct extension of their mechanism of action, cause severe lactic acidosis. This is not very common at least not as common as it was with phenformin but it still happens, particularly where metformin accumulates due to renal failure. Its other side effects consist of gastro-abdominal stuff, for example a metallic taste in your mouth, diarrhoea, abdominal discomfort, anorexia, etc.
Sulfonylureas have a distinct tendency to cause undesirable hypoglycaemia, which is a direct extension of their therapeutic effect. They stimulate insulin secretion no matter the glucose concentration, and therefore remove the normal regulatory safeguards that prevent insulin release during periods of normal and low blood glucose.
The result is essentially an insulin overdose. Other side effects can include hypokalemia, weight gain, skin eruptions and photosensitivity. α-glucosidase inhibitors are essentially osmotic laxatives, as their mechanism of action is centered on creating malabsorption.
They leave a lot of unfinished carbohydrate scraps in the lumen of the bowel, and as you might imagine, there are plenty of microbial scavengers down there who are ready to pounce on these molecules, gladly metabolising them into clouds of flatus and torrents of diarrhoea.
These are potentially dinner-party-ending consequences, as these drugs are taken immediately at the commencement of a meal.
Meglitinides , like sulfonylureas, directly stimulate the release of insulin, but because they are very short-acting and taken immediately before a meal, the possibility of severe hypoglycaemia is somewhat diminished. Other weird, unexpected adverse effects in studied populations were headaches, and an increased risk of upper respiratory tract infections - for some reason specifically sinusitis.
Thiazolidinediones are generally not likely to cause life-threatening hypoglycaemia, even though they increase insulin sensitivity.
Unfortunately, by making adipose tissue more interested in glucose, they make it grow in size, and noticeable weight gain results. They also effect PPAR receptors in bone, and are associated with an increase in the risk of fracture.
PPAR activation in renal tubular cells, on the other hand, leads to fluid retention, and oedema results. Additionally, individual agents have distinct and unpleasant risk profiles: rosiglitazone is associated with myocardial ischaemia and pioglitazone slightly increases the risk of bladder cancer.
Dipeptidyl peptidase DPP-4 inhibitors have a fairly benign side effect profile. They are generally said to be "weight-neutral", i.
the population of patients starting sitagliptin therapy remain as obese as they were before treatment. The incidence of serious hypoglycaemia with this class is also fairly low.
The most commonly reported adverse effects were sinus infections and headache. GLP-1 receptor agonists are also rather free from serious life-threatening side effects, with the exception of some idiosyncratic pancreatitis episodes reported with exenatide. Nausea and anorexia are also reported.
SGLT-2 inhibitors are basically osmotic diuretics, and have a tendency to produce polyuria and volume depletion.
At the same time the urine becomes sweeter, and the incidence of urinary tract infection increases. The most interesting side effect is probably euglycaemic ketoacidosis , where a sustained low BSL produces a downregulation of insulin release and a concomitant increase in ketogenic hormones like glucagon adrenaline and cortisol.
Lorenzati, Bartolomeo, et al. Kimmel, Bonnie, and Silvio E. Fowler, Michael J. Bailey, Clifford J. Watanabe, C. Influence of injected guanidine hydrochloride upon blood sugar content. Blanchard, Tiphaine, et al. in horses. Selizer, H. Srivastava, Manoj K. Blackburn, Henry, and David R. Jacobs Jr.
Gale, Edwin. Review of the first available 3rd generation sulphonylurea. Lang, Veronica, and Peter E. Guardado-Mendoza, Rodolfo, et al.
Yki-Järvinen, Hannele. Yasmin, Sabina, and Venkatesan Jayaprakash. Cheatham, Wayman Wendell. Fujita, Takeshi, et al. Malaisse, Willy J. Baetta, Roberta, and Alberto Corsini. Hinnen, Deborah. Eng, John, et al. Further evidence for an exendin receptor on dispersed acini from guinea pig pancreas.
Rieg, Timo, and Volker Vallon. Kalra, Sanjay. Rena, Graham, D. Grahame Hardie, and Ewan R. Sola, Daniele, et al. Derosa, Giuseppe, and Pamela Maffioli. Puls, W. Springer, Berlin, Heidelberg, Karger Publishers, Berger, Joel, and David E. Thornberry, Nancy A. Cornell, Susan. Brunton, S. Dardi, I.
Kouvatsos, and S. Laube, Heiner. Breadcrumb Deranged Physiology CICM Primary Exam Required Reading Endocrine System. Pharmacology of oral hypoglycaemic drugs.
Previous chapter: Pharmacology of insulin preparations and glucagon Next chapter: Pharmacology of vasopressin and its analogues. All SAQs related to this topic.
All vivas related to this topic. Those questions, for the record, were: Question 6 from the second paper of Question 6 from the first paper of Examiner comments emphasised the need for "a strong and logical structure" and "more correct information" , which seem like reasonable expectations.
Class mechanism of action Adverse effects Biguanides: By disabling the mitochondrial respiratory chain, decrease the ATP supply to hepatocytes, activating AMPK a fuel-sensing enzyme which regulates the balance of anabolic and catabolic activity.
The depolarisation then leads to insulin release - undesirable severe hypoglycaemia - hypokalemia - secondary failure of therapy as beta-cells burn out - erythema multiforme - exfoliative dermatitis - photosensitivity α-glucosidase inhibitors: By acting as a pseudocarbohydrate, they substitute themselves as a substrate for α-glucosidase enzymes such as sucrase, maltase, dextranase and glucoamylase, which results in decreased intestinal absorption of complex carbohydrates - malabsorption of carbohydrates - diarrhoea - flatulence - abdominal bloating Meglitinides: By binding to the ATP-sensitive K channel, meglitinides act like ATP i.
The depolarisation then leads to insulin release - undesirable severe hypoglycaemia but less likely than with sulfonylureas - respiratory tract infections - headache Thiazolidinediones: PPARγ receptor activation leads to the increased synthesis and activity of cellular proteins involved in glucose uptake and processing, which results in an increased effect from any insulin binding in insulin-sensitive tissues espeically adipocytes.
The result is an increase in insulin sensitivity - weight gain - increased risk of bone fractures - fluid retention and oedema - cardiac ischaemia rosiglitazone only DPP-4 inhibitors: By decreasing the degradation of GLP-1, DPP-4 inhibitors produce an increase in insulin secretion.
This request occurred following more than 60 reports of severe liver toxicity in patients taking this agent. A majority of the data reporting the efficacy of this class comes from studies with troglitazone, although results from more recent studies with the newer agents rosiglitazone and pioglitazone demonstrate similar properties.
These agents have a notable effect on improving insulin resistance, particularly when used in combination with other antidiabetic drugs, but have no effect on insulin secretion. Monotherapy with these agents has been associated with a 0. Results from studies with troglitazone consistently show a decrease in triglyceride levels—in some cases by as much as 33 percent.
Patients treated with pioglitazone have displayed mean decreases in triglyceride levels, mean increases in HDL cholesterol levels, and no consistent mean changes in LDL and total cholesterol levels. Because these agents do not increase insulin secretion, hypoglycemia does not pose a risk when thiazolidinediones are taken as monotherapy.
Significant weight gain has been reported with all three agents. The thiazolidinediones are relatively safe in patients with impaired renal function because they are highly metabolized by the liver and excreted in the feces; however, caution should be used in patients with hepatic dysfunction because troglitazone and its metabolites have been shown to accumulate in this setting.
The manufacturers recommend that these agents not be prescribed for patients with serum transaminase levels that exceed 2. Mild to moderate edema has been reported in 5 to 7 percent of patients treated with rosiglitazone and pioglitazone. The use of thiazolidinediones should be avoided in these patients.
As referred to earlier, of greatest concern are the reports of an idiosyncratic drug reaction with troglitazone. This reaction is initially characterized by increased serum transaminase levels, which in some cases progressed to hepatitis, hepatic failure and death.
Preliminary attempts before troglitazone was withdrawn from the market in March to prevent such incidents included a request by the FDA that Parke-Davis strengthen the drug's labeling and require stringent monitoring of transaminase levels in patients taking this agent.
In March , the FDA's Endocrine and Metabolic Drugs Advisory Committee reviewed the status of troglitazone and the potential toxicities and recommended continued availability in a select group of patients: those who are not well controlled with other antidiabetic agents. Since then, it has been determined that patients requiring the use of an insulin sensitizer should be treated with one of the alternative agents.
Although results from pre-marketing trials revealed no evidence of hepatotoxicity with the newer agents rosiglitazone and pioglitazone , two recent case reports demonstrated that rosiglitazone may be associated with hepatic failure following just 14 days of therapy, although a true cause-and-effect relationship has not been established.
The FDA recommends that serum transaminase levels be monitored every other month for the first year in all patients receiving a thiazolidinedione. Following one year of therapy with the newer agents, the incidence of serum transaminase elevations has been reported to be similar to placebo.
The time to achieve a desired effect with the thiazolidinediones is somewhat longer than the other classes of hypoglycemic agents discussed thus far. Intervals of at least three to four weeks should be allowed before increasing the dosage of these agents. Smaller dosages can be initiated if used as part of a combination regimen with a sulfonylurea or a sulfonylurea plus metformin.
In patients receiving insulin therapy, the addition of a thiazolidinedione has resulted in significant reductions in daily insulin requirements.
Acarbose Precose and miglitol Glycet are the two agents available in this class. Alpha-glucosidase inhibitors act by inhibiting the enzyme alpha-glucosidase found in the brush border cells that line the small intestine, which cleaves more complex carbohydrates into sugars.
Because they inhibit the breakdown and subsequent absorption of carbohydrates dextrins, maltose, sucrose and starch; no effect on glucose from the gut following meals, the largest impact of these drugs is on postprandial hyperglycemia. Their effect on FPG levels is modest. They have been associated with a reduction in HbA 1c by 0.
The most bothersome side effects observed with these agents are gastrointestinal, including abdominal discomfort, bloating, flatulence and diarrhea but are reversible with discontinuation. Therapy with acarbose has been linked to elevations in serum transaminase levels and the use of this agent is contraindicated in patients with liver cirrhosis.
Likewise, concentrations of the alpha-glucosidase inhibitors have been shown to increase proportionally to the degree of renal dysfunction and their use in patients with a serum creatinine level more than 2. Other contraindications include patients with inflammatory bowel disease or a history of bowel obstruction.
Therapy should be initiated with the lowest effective dose and titrated slowly over intervals of two to four weeks. Patients should be instructed to take this medication with food. For maximum efficacy, the dietary carbohydrate intake should exceed 50 percent. Although hypoglycemia is not typically associated with monotherapy with the alpha-glucosidase inhibitors, it can occur in combination with other drugs.
It is important, therefore, to inform patients that the traditional treatment for hypoglycemia may be blocked while using this therapy and to consume only glucose.
If adequate control is not obtained with the use of a single agent, combination therapy is an option Figure 1.
Several of the available oral agents have been studied in combination and have been shown to further improve glycemic control when compared to monotherapy. Reasonable combinations of agents include a sulfonylurea plus metformin, a sulfonylurea plus an alpha-glucosidase inhibitor, a sulfonylurea plus a thiazolidinedione, metformin plus repaglinide, biguanide plus alpha-glucosidase inhibitor, and metformin plus a thiazolidinedione.
A newer formulation Glucovance combines glyburide and metformin in one tablet, allowing a more convenient dosing schedule. Some physicians advocate therapy combining three oral agents, sulfonylurea, metformin, thiazolidinedione or sulfonylurea, metformin, alpha-glucosidase inhibitor , although this approach has not been extensively studied.
Several other combinations have recently been reviewed. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, etal. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U. S adults.
The Third National Health and Nutrition Examination Survey, — Diabetes Care. Nathan DM, Kitrick C, Larkin M, Schaffran R, Singer DE. Glycemic control in diabetes mellitus: have changes in therapy made a difference?.
Am J Med. United Kingdom Prospective Diabetes Study UKPDS Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes UKPDS DeFronzo RA.
Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. Feinglos MN, Bethel MA. Treatment of type 2 diabetes mellitus. Med Clin North Am. American Diabetes Association. The pharmacological treatment of hyperglycemia in NIDDM. Berger M, Jorgens V, Muhlhauser I. Rationale for the use of insulin therapy alone as the pharmacological treatment of type 2 diabetes.
Luna B, Hughes AT, Feinglos MN. The use of insulin secretagogues in the treatment of type 2 diabetes. Prim Care.
Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Therapy of type 2 diabetes, cardiovascular death, and the UGDP. Am Heart J. Meinert CL, Knatterud GL, Prout TE, Klimt CR. A study of the effects of hypoglycemic agents on vascular complications in patients with adult-onset diabetes.
Mortality results. Gerich JE. Oral hypoglycemic agents. N Engl J Med. DeFronzo RA, Goodman AM. Efficacy of metformin in patients with non-insulin-dependent diabetes mellitus. The Multicenter Metformin Study Group.
Stumvoll M, Nurjhan N, Perriello G, Dailey G, Gerich JE. The metabolic effects of metformin in non-insulin-dependent diabetes mellitus. Hermann LS, Schersten B, Bitzen PO, Kjellstrom T, Lindgarde F, Melander A.
Therapeutic comparison of metformin and sulfonylurea, alone and in various combinations. A double-blind controlled study. Campbell IW, Menzies DG, Chalmers J, McBain AM, Brown IR. One year comparative trial of metformin and glipizide in type 2 diabetes mellitus. Diabetes Metab.
Dornan TL, Heller SR, Peck GM, Tattersall RB. Double-blind evaluation of efficacy and tolerability of metformin in NIDDM. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes UKPDS Nolan JJ, Jones NP, Patwardhan R, Deacon LF.
Rosiglitazone taken once daily provides effective glycaemic control in patients with type 2 diabetes mellitus. Diabet Med. Raskin P, Rappaport EB, Cole ST, Yan Y, Patwardhan R, Freed MI.
Rosiglitazone short-term monotherapy lowers fasting and post-prandial glucose in patients with type II diabetes. Saltiel AR, Olefsky JM. Thiazolidinediones in the treatment of insulin resistance and type II diabetes.
Ghazzi MN, Perez JE, Antonucci TK, Driscoll JH, Huang SM, Faja BW, etal. Cardiac and glycemic benefits of troglitazone treatment in NIDDM. The Troglitazone Study Group. Forman LM, Simmons DA, Diamond RH.
Hepatic failure in a patient taking rosiglitazone. Al-Salman J, Arjomand H, Kemp DG, Mittal M. Hepatocellular injury in a patient receiving rosiglitazone.
A case report. Schwartz S, Raskin P, Fonseca V, Graveline JF.
New hypoglycemic drugs, including glucagon-like peptide 1 receptor agonists GLP-1RA hypoglycemi, dipeptidyl peptidase-4 inhibitors DPP-4i and sodium-glucose cotransporter Orral inhibitors SGLT-2iDrufs brings more options for Iron status and immune function in athletes treatment Oarl type Healthy dessert options diabetes T2DM. Druga are generally well tolerated, although caution is required in Herbal tea for stress cases. Herbal tea for stress trials have hypoglycejic good glycemic control with combination therapy with new hypoglycemic drugs in prediabetes and T2DM mostly traditional stepwise therapybut early combination therapy appears to have faster, more, and longer-lasting benefits. Clinical and preclinical studies support that SGLT-2i exerts its protective effect on heart failure through indirect and direct effects. How this comprehensive protective effect regulates the dynamic changes of heart genes needs further study. According to IDF diabetes atlas 10th edition: Globally, 1 out of every 10 adults aged 20—79 have diabetes. It is estimated that by andthis number will increase to million and million, respectively.
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