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Semaglutide Correct Use
By: Road2HardCoreIron Date: April 8, 2023, 7:52 am
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(Dose varies Person)**********
Semaglutide
Description
Semaglutide is a recombinant DNA produced polypeptide analogue
of human glucagon-like peptide-1 (GLP-1) which is used in
combination with diet and exercise in the therapy of type 2
diabetes, either alone or in combination with other antidiabetic
agents. There have been no published reports of hepatotoxicity
attributed to semaglutide therapy.
Semaglutide is a polypeptide that contains a linear sequence of
31 amino acids joined together by peptide linkages. It is an
agonist of glucagon-like peptide-1 receptors (GLP-1 AR) and used
for the treatment of type 2 diabetes. It has a role as a
hypoglycemic agent, a glucagon-like peptide-1 receptor agonist,
an anti-obesity agent, a neuroprotective agent and an appetite
depressant. It is a polypeptide and a lipopeptide.
Obesity is a global health challenge with few pharmacologic
options. Whether adults with obesity can achieve weight loss
with once-weekly semaglutide at a dose of 2 mg as an adjunct to
lifestyle intervention has not been confirmed.
Semaglutide (Glucagon-Like Peptide-1) Overview
Semaglutide, GLP-1, short for glucagon-like peptide-1 is a
short, naturally occurring peptide hormone just 30-31 amino
acids in length. Its primary physiologic function is to lower
blood sugar levels by naturally enhancing insulin secretion. It
also plays roles in protection beta cell insulin stores by
promoting insulin gene transcription and has been linked with
neurotrophic effects in the brain and central nervous system.
In the GI system, GLP-1 has been shown to significantly decrease
appetite by delaying gastric emptying and reducing intestinal
motility. Preliminary research has shown impacts of GLP-1 in the
heart, fat, muscles, bones, liver, lungs, and kidneys as well.
The primary focus of GLP-1 research has been in the realm of
diabetes treatment/prevention as well as appetite suppression.
Secondary research focuses on the potential cardiovascular
benefits of the peptide. More recent, and thus less robust,
research focuses on the ability of GLP-1 to stave off
neurodegenerative disease. Though this latter area of research
is newest, it is also the fast-growing area of GLP-1 study now
that the peptide has been revealed to slow or prevent the
accumulation of amyloid beta plaques in the setting of
Alzheimer’s disease.
Semaglutide is a glucagon-like peptide-1 receptor agonist. It
increases the production of insulin, a hormone that lowers the
blood sugar level. It also appears to enhance growth of β
cells in the pancreas, which are the sites of insulin
production.
In short, it inhibits glucagon, which is a hormone that
increases blood sugar. It additionally reduces food intake by
lowering appetite and slows down digestion in the stomach. In
this way it reduces body fat.
Semaglutide GLP-1 research
The Incretin Effect of GLP-1
Perhaps the most important effect that GLP-1 has, according to
Dr. Holst, is referred to as the “incretin effect.” Incretins
are a group of metabolic hormones, released by the GI tract,
that cause a decrease in blood glucose (sugar) levels. GLP-1 has
been shown to be one of the two most important hormones (the
other being GIP) to stimulate the incretin effect in rodent
models. Though GIP circulates at levels roughly 10 times higher
than that of GLP-1, there is evidence that GLP-1 is the more
potent of the two molecules, particularly when levels of blood
glucose are quite high.
A GLP-1 receptor has been identified on the surface of
pancreatic beta cells, making it clear that GLP-1 directly
stimulates the exocytosis of insulin from the pancreas. When
combined with sulfonylurea drugs, GLP-1 has been shown to boost
insulin secretion enough to cause mild hypoglycemia in up to 40%
of subjects[1]. Of course, increased insulin secretion is
associated with a number of trophic effects including increased
protein synthesis, reduction in the breakdown of protein, and
increased uptake of amino acids by skeletal muscle.
GLP-1 and Beta Cell Protection
Research in animal models suggests that GLP-1 can stimulate the
growth and proliferation of pancreatic beta cells and that it
may stimulate the differentiation of new beta cells form
progenitors in the pancreatic duct epithelium. Research has also
shown that GLP-1 inhibits beta cell apoptosis. Taken in sum,
these effects tip the usual balance of beta cell growth and
death toward growth, suggesting that the peptide may be useful
in treating diabetes and in protecting the pancreas against
insult that harms beta cells.
In one particularly compelling trial, GLP-1 was shown to inhibit
the death of beta cells caused by enhanced levels of
inflammatory cytokines. In fact, mouse models of type 1 diabetes
have revealed that GLP-1 protects islet cells from destruction
and may, in fact, be a useful means of preventing onset of the
type 1 diabetes.
GLP-1 and Appetite
Research in mouse models suggests that administration of GLP-1,
and its similar cousin GLP-1, into the brains of mice can reduce
the drive to eat and inhibit food intake. It appears that GLP-1
may actually enhance feelings of satiety, helping individuals to
feel fuller and reducing hunger indirectly. Recent clinical
studies have shown in mice that twice daily administration of
GLP-1 receptor agonists cause gradual, linear weight loss. Over
a long period, this weight loss is associated with significant
improvement in cardiovascular risk factors and a reduction in
hemoglobin A1C levels, the latter of these being a proxy marker
for the severity of diabetes and the quality of blood sugar
control attained via treatment.
Potential Cardiovascular Benefits of GLP-1
It is now know that GLP-1 receptors are distributed throughout
the heart and act to improve cardiac function in certain
settings by boosting heart rate and reducing left ventricular
end-diastolic pressure. The latter may not seem like much, but
increased LV end-diastolic pressure is associated with LV
hypertrophy, cardiac remodeling, and eventual heart failure.
Recent evidence has even suggested that GLP-1 could play role in
decreasing the overall damaged caused by a heart attack. It
appears that the peptide improves cardiac muscle glucose uptake,
thereby helping struggling ischemic heart muscle cells to get
the nutrition they need to continue functioning and avoid
programmed cell death. The increase in glucose uptake in these
cells appears to independent of insulin.
Large infusions of GLP-1 into dogs have been shown to improve LV
performance and reduce systemic vascular resistance. The latter
effect can help to reduce blood pressure and ease strain on the
heart as a result. This, in turn, can help to reduce the
long-term consequences of high blood pressure such as LV
remodeling, vascular thickening, and heart failure. According to
Dr. Holst, administration of GLP-1 following cardiac injury has
“constantly increased myocardial performance both in
experimental animal models and in patients.”
GLP-1 and the Brain
There is some evidence to suggest that GLP-1 can improve
learning and help to protect neurons against neurodegenerative
diseases such as Alzheimer’s disease. In one study, GLP-1 was
shown to enhance associative and spatial learning in mice and
even to improve learning deficits in mice with specific gene
defects. In rats that over-express the GLP-1 receptor in certain
regions of the brain, learning and memory are both significantly
better than in their normal controls.
Additional research in mice has shown that GLP-1 can help to
protect against excitotoxic neuron damage, completely protecting
rat models of neurodegeneration against glutamate-induced
apoptosis. The peptide can even stimulate neurite outgrowth in
cultured cells. Researchers are hopeful that additional research
on GLP-1 will reveal how it might be used to halt or reverse
certain neurodegenerative diseases.
Interestingly, GLP-1 and its analogue exendin-4 have been shown
in mouse models to reduce levels of amyloid-beta in the brain as
well as the beta-amyloid precursor protein found in neurons.
Amyloid beta is the primary component of the plaques observed in
Alzheimer’s disease, plaques which, while not necessarily known
to be causative, are associated with the severity of the
disease. It remains to be seen if preventing amyloid beta
accumulation can protect against the effects of Alzheimer’s
disease, but this research is, at the very least, a tantalizing
clue as to how scientists my intervene in the progression of
mild cognitive impairment to full Alzheimer’s disease.
GLP-1 exhibits minimal to moderate side effects, low oral and
excellent subcutaneous bioavailability in mice. Per kg dosage in
mice does not scale to humans.
Semaglutide Questions
• How to use semaglutide for weight loss?
Taking 2.4 Mg/0.75 Ml Subcutaneous Pen Injector as example,
inject this medication under the skin in the thigh, abdomen, or
upper arm as directed by your doctor, usually once weekly. It
may be used with or without food. The dosage is based on your
medical condition and response to treatment. Your doctor will
start you on a low dose first to decrease your risk of
stomach/abdominal side effects, and gradually increase your
dose. Follow your doctor’s instructions carefully.
Before using, check this product visually for particles or
discoloration. If either is present, do not use the liquid.
Before injecting each dose, clean the injection site with
rubbing alcohol. Change the injection site each time to lessen
injury under the skin. Do not inject in an area that is tender,
bruised, red, hard, or has scars or stretch marks.
Use this medication regularly to get the most benefit from it.
To help you remember, use it on the same day and time each week.
It may help to mark your calendar with a reminder. Carefully
follow the meal plan and exercise program your doctor has
recommended. Learn how to store and discard medical supplies
safely.
• How does semaglutide burn fat?
Patients can lose significant weight on semaglutide because it
suppresses appetite. Semaglutide can be taken orally or by
injection, according to Novo Nordisk, and it works by increasing
the production of insulin, a hormone produced by the pancreas
that helps regulate blood sugar.
What are the side effects of semaglutide?
Semaglutide injection may cause side effects. Tell your doctor
if any of these symptoms are severe or do not go away: nausea.
vomiting. diarrhea. abdominal pain. constipation. heartburn.
burping.
Does semaglutide cause hair loss?
No, hair loss wasn’t reported as a side effect by people taking
Ozempic in clinical studies. But hair loss and hair thinning may
occur in people who have diabetes and consistently high blood
sugar levels. If you have questions about hair loss, talk with
your doctor or pharmacist.
How quickly do you lose weight with semaglutide?
Despite the promising research, there’s one major caveat to the
medication: in order to keep the weight off, patients need to
continue taking it. One recent study showed that patients on
semaglutide lost 10% of their body weight in 20 weeks, but
regained nearly all of it after the treatment.
How long do you stay on semaglutide?
Most patients will start semaglutide treatment at the lower 0.25
mg dose injected once a week for 4 weeks. The 0.25 mg dose is
not used as your final maintenance dose to lower your blood
sugar.
Where do you inject semaglutide?
If you will be using semaglutide at home, your doctor will teach
you how the injections will be given. Be sure you understand
exactly how the medicine is to be injected. This medicine is
given as a shot under the skin of your stomach, thighs, or upper
arm. Use a different body area each time you give yourself a
shot.
Does semaglutide make tired?
Swelling/redness/itching at the injection site, tiredness,
nausea, vomiting, diarrhea, or constipation may occur. Nausea
usually lessens as you continue to use semaglutide. If any of
these effects last or get worse, tell your doctor or pharmacist
promptly. Other adverse reactions with a frequency of >0.4% were
associated with OZEMPIC include fatigue, dysgeusia and
dizziness.
What happens when you stop semaglutide?
Continuation of semaglutide after 20 weeks of initial therapy
leads to significant continued weight loss, according to a new
study, but stopping the therapy causes patients to regain much
of the weight they initially lost.
Is semaglutide safe long term?
The study demonstrates that long-term use of oral semaglutide
with flexible dose adjustment results in durable improvements in
glycemic control and further reductions in body weight and is
generally well tolerated.
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