Why Ozempic Causes Blindness?

What Is Ozempic?

Ozempic (semaglutide) Injection is a glucagon-like peptide 1 (GLP-1) receptor agonist indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.

What Are Side Effects of Ozempic?

Ozempic may cause serious side effects including:

• a lump in the neck,
• difficulty swallowing,
• cough,
• shortness of breath,
• difficulty breathing,
• upper abdominal pain,
• nausea,
• vomiting,
• blurred vision,
• spots or dark strings floating in your vision,
• fluctuating vision,
• vision loss,
• dark or empty areas in your vision,
• shakiness,
• nervousness,
• anxiety,
• sweating,
• chills,
• clamminess,
• irritability,
• impatience,
• confusion,
• fast heartrate,
• lightheadedness,
• dizziness,
• hunger,
• decreased urination,
• swelling in your legs, ankles, or feet,
• fatigue,
• rash,
• itching, and
• shock

Get medical help right away, if you have any of the symptoms listed above.

Common side effects of Ozempic include:

• nausea,
• vomiting,
• diarrhea,
• abdominal pain and constipation.

Seek medical care or call 911 at once if you have the following serious side effects:

• Serious eye symptoms such as sudden vision loss, blurred vision, tunnel vision, eye pain or swelling, or seeing halos around lights;
• Serious heart symptoms such as fast, irregular, or pounding heartbeats; fluttering in your chest; shortness of breath; and sudden dizziness, lightheadedness, or passing out;
• Severe headache, confusion, slurred speech, arm or leg weakness, trouble walking, loss of coordination, feeling unsteady, very stiff muscles, high fever, profuse sweating, or tremors.

Ozempic is an analogue to glucagon-. The glucagon-like peptide-1 receptor (GLP1R) is a G protein-coupled receptor (GPCR) found on beta cells of the pancreas and on neurons of the brain. It is involved in the control of blood sugar level by enhancing insulin secretion.

GLP1R binds glucagon-like peptide-1 (GLP1) and glucagon as its natural endogenous agonists.^[14]

Agonists:

·         GLP-1 – endogenous in humans^[14]

·         glucagon – endogenous in humans^[14]

·         oxyntomodulin

·         exendin-4,^[14][15]

·         exenatide

·         lixisenatide^[14]

·         albiglutide

·         beinaglutide

·         dulaglutide

·         efpeglenatide

·         langlenatide

·         liraglutide^[14]

·         PEG- Loxenatide

·         semaglutide

·         taspoglutide

·         Ecnoglutide

·         Utreglutide

·         Glepaglutide

·         Apraglutide

·         Maridebart Cafraglutide/AMG133

·         Tirzepatide

·         pegapamodutide

·         Mazdutide

·         Survodutide

·         Bamadutide

·         Pemvidutide

·         Cotadutide

·         Retatrutide

·         lithium chloride

·         Grutalumab

·         DA1726

·         GX-G6

·         GZR18

·         HRS9531

·         BGMO504

·         PB718

·         RAY1225

·         VCT220

·         VK2735

 

The GLP-1 receptor is a transmembrane protein composed of seven alpha-helical transmembrane domains (TM1-TM7), an extracellular N-terminus, and an intracellular C-terminus. It belongs to the class B family of G protein-coupled receptors, also known as secretin-like receptors. The N-terminus of the receptor is responsible for binding glucagon-like peptide-1 (GLP-1) ligands, while the intracellular C-terminus interacts with intracellular signaling proteins to initiate downstream signaling pathways.

The extracellular N-terminus contains key regions involved in ligand recognition and binding. It undergoes conformational changes upon ligand binding, leading to activation of intracellular signaling cascades. The intracellular C-terminus interacts with G proteins and other signaling molecules to initiate cellular responses.

Glucagon-like peptide-1 (GLP-1) is a hormone consisting of 30 amino acids. It is released by intestinal L cells when nutrients are consumed. GLP-1 has multiple effects, including enhancing insulin secretion from pancreatic beta cells in response to glucose, increasing insulin expression, preventing beta-cell apoptosis, promoting the formation of new beta cells, reducing glucagon secretion, slowing down stomach emptying, promoting satiety, and improving glucose disposal in peripheral tissues. Due to these diverse effects, there has been significant interest in developing long-lasting agonists of the GLP-1 receptor (GLP-1R) for the treatment of type 2 diabetes (T2D).

GLP1R is also expressed in the brain^[18] where it is involved in the control of appetite.^[19] Furthermore, mice that over express GLP1R display improved memory and learning.^[20]

Stretch responsive vagal neurons in the stomach and intestines also express GLP1R.^[21] GLP1R neurons particularly and densely innervate stomach muscle and can communicate with additional organ systems changing breathing and heart rate due to activation.^[21]

Upon binding to its ligand GLP-1, the GLP-1 receptor activates intracellular signaling pathways that regulate insulin secretion, glucose metabolism, and satiety. In pancreatic beta cells, GLP-1 receptor activation enhances glucose-stimulated insulin secretion. This occurs through the activation of adenylyl cyclase, leading to increased intracellular levels of cyclic AMP (cAMP). The rise in cAMP activates protein kinase A (PKA), which promotes insulin exocytosis and enhances beta cell survival and proliferation. GLP-1 receptor signaling in pancreatic alpha cells reduces glucagon secretion, further contributing to glucose lowering. By inhibiting glucagon release, GLP-1 receptor activation helps to maintain glucose homeostasis. Another important function of the GLP-1 receptor is the regulation of gastric emptying. Activation of the receptor delays the rate at which the stomach empties, leading to increased satiety and reduced food intake. This effect contributes to weight management and appetite control.

'Appetite regulation and satiety': GLP-1 receptor signaling influences the central nervous system, particularly regions involved in appetite regulation. Activation of the GLP-1 receptor promotes feelings of satiety, leading to a reduction in food intake and improved weight management.

Gastric emptying': GLP-1 receptor activation slows down the rate at which the stomach empties its contents into the small intestine. This delay in gastric emptying contributes to the feeling of fullness and aids in controlling postprandial blood glucose levels.

 

The fact that semaglutide binds to a receptor in central nervous system and it is a ligand which structurally is a peptide, which is slightly different from GLP-1, leads us to the conclusion that if this peptide in connection to other protein (such as the GLP-1 receptor) induces an autoimmune reaction against the bounded semaglutide, the antibodies against this bounded semaglutide may react also to normal nervous cells which are bounded with normal GLP-1, which is regularly produced by our own intestinal cells.

Why the immune system attacks our nerve cells, particularly the cells of nervus opticus is only a question of time to be explained. Perhaps this is only the top of the iceberg.