Well & Wild

Well & Wild As an endocrinologist and obesity expert, I have specialised in metabolic diseases, obesity and diabetes for 30 years.

I have led many clinical trials and published many academic papers related to obesity.

06/01/2025

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After taking it, it will first start to diffuse in the digestive tract and gradually enter the blood circulation system....
05/06/2025

After taking it, it will first start to diffuse in the digestive tract and gradually enter the blood circulation system. Thanks to its own chemical structure and physicochemical properties, it can “ride” on the “high-speed transportation channel” of blood flow in a stable and biologically active form, and smoothly reach target organs and tissues throughout the body. Performs the “magic” of delaying gastric emptying. Slows down the rate of food evacuation from the stomach into the small intestine, allowing carbohydrates and other nutrients to enter the intestines gradually to be absorbed, avoiding “steep spikes” in postprandial blood glucose, and smoothing out the curve of blood glucose fluctuations. After crossing the blood-brain barrier, Meglutide participates in the activity of the appetite regulation center. Here, it “tweaks” the balance of neural signals, releases satiety signals, suppresses hunger, cuts down on the desire to eat, controls calorie intake from the source, and helps stabilize blood glucose in a reasonable range.

Storage and Breakdown of FatFats in food consumed by the body are broken down during digestion into fatty acids and glyc...
05/06/2025

Storage and Breakdown of Fat
Fats in food consumed by the body are broken down during digestion into fatty acids and glycerol, which enter the bloodstream and are transported throughout the body. Excess fatty acids are synthesized into triglycerides in the liver and fat cells and then stored. When we consume too many calories, the body stores this excess fat as adipose tissue for use during times of high energy demand.
Storage: When we eat, fat is broken down in the intestines, and fatty acids and glycerol enter the bloodstream. They are transported through the bloodstream to adipose tissue, where they are converted into triglycerides and stored in fat cells. This process is regulated by hormones such as insulin, which prompts fat cells to combine fatty acids and glycerol to form triglycerides and store them.
Catabolism: Fat stores are mobilized when the body needs energy (e.g., during exercise or hunger). Hormones such as adrenaline and noradrenaline activate lipolytic enzymes in fat cells that begin to break down stored triglycerides into fatty acids.
Release and Transport of Fatty Acids
Broken-down fatty acids are transported through the bloodstream to the liver, muscles, and other tissues that use fatty acids as an energy source. Fatty acids can be transported where they are needed for energy via fatty acid-binding proteins (FABP) and plasma proteins such as albumin.
Muscles: During exercise, muscle cells have a high energy demand, especially during aerobic exercise, and fat becomes an important energy source. Fatty acids enter the muscle cell and are broken down into carbon dioxide and water through the process of "beta-oxidation" in the mitochondria, which also releases ATP (cellular energy).
Liver: Fatty acids also enter the liver, where liver cells convert them through fatty acid oxidation into ketone bodies, which serve as an energy source for the brain and other tissues, especially during long periods of fasting or on a low-carbohydrate diet like the ketogenic diet.
β-Oxidation (Process of Fatty Acid Oxidation)
In the cells, fatty acids enter the mitochondria and undergo β-oxidation, which is the primary catabolic process for fatty acids. Each oxidation process removes two carbon atoms to create an acetyl-coenzyme A (acetyl-CoA). These acetyl-coenzyme A molecules enter the tricarboxylic acid cycle (also known as the Krebs cycle) and ultimately pass through the respiratory chain to produce ATP. This process is the central step in the energy-providing process for fats.
Production and Use of Ketone Bodies
When the body is exposed to prolonged fasting or low carbohydrate intake, the liver converts fatty acids into ketone bodies. Ketone bodies (including acetoacetic acid, beta-hydroxybutyric acid, and acetone) are a highly efficient energy source, especially for the brain. Normally, the brain relies primarily on glucose, but during periods of starvation, it uses ketone bodies as an alternative energy source.
Regulation of Fat Metabolism
Fat metabolism is regulated by a variety of hormones and enzymes. Here are some key regulators:
Insulin: Insulin is the main storage hormone in fat metabolism. When blood sugar levels are high, insulin secretion increases, promoting fat storage. Insulin inhibits lipolysis and helps store energy as fat.
Epinephrine and Norepinephrine: These hormones are released in response to stress, exercise, or hunger and promote the breakdown of fat, releasing fatty acids into the bloodstream.
Growth Hormone: This hormone is important during childhood growth; it also helps with the breakdown of fat and promotes the release of fatty acids.
Testosterone and Estrogen: S*x hormones also affect fat distribution and metabolism. For example, testosterone contributes to fat burning, while estrogen can promote fat storage in certain areas, such as the thighs and buttocks.

Lipedema: Troubles Caused by Fat Metabolism ImbalanceLipedema is a chronic disease that mainly affects the lower extremi...
05/06/2025

Lipedema: Troubles Caused by Fat Metabolism Imbalance
Lipedema is a chronic disease that mainly affects the lower extremities. It is characterized by abnormal and uneven accumulation of adipose tissue. This condition often presents bilaterally symmetrically, usually starting from the distal part of the legs and gradually spreading upwards.
Lymphedema: Swelling Caused by Obstructed Lymphatic Circulation
Lymphedema occurs due to a dysfunction in the lymphatic system, which leads to poor lymphatic fluid drainage. Excessive lymphatic fluid accumulates in the interstitial spaces, thereby causing local or systemic swelling.

I am a Professor of Medicine at the University of Toronto, where my research includes long-term complications of diabete...
05/06/2025

I am a Professor of Medicine at the University of Toronto, where my research includes long-term complications of diabetes, evaluation of new therapies for type 1 and type 2 diabetes, and I am a recipient of the ADA Distinguished Physician-Clinician Award, the CDA Lifetime Achievement Award, and the Novartis Diabetes Award in 2009, and the ADA Award for Outstanding Achievement in Clinical Diabetes Research in 2020.

GLP-1 (Glucagon-Like Peptide-1) er et naturlig forekommende peptidhormon som har en rekke fysiologiske roller i menneske...
05/06/2025

GLP-1 (Glucagon-Like Peptide-1) er et naturlig forekommende peptidhormon som har en rekke fysiologiske roller i menneskekroppen, først og fremst knyttet til insulinsekresjon, blodsukkerregulering og vektkontroll. GLP-1s virkninger er ofte nært knyttet til blodsukkerregulering og mage-tarmkanalens funksjon, og har derfor et bredt spekter av bruksområder innen behandling av diabetes og fedme.
De viktigste effektene av GLP-1:
Fremmer insulinsekresjon: GLP-1 fremmer insulinsekresjon etter spising, spesielt når blodsukkernivået er forhøyet, noe som bidrar til å senke det postprandiale blodsukkernivået.
Undertrykker tømming av magesekken: GLP-1 bremser tømmingen av mageinnholdet, noe som gjør at du føler deg mett og bidrar til å redusere mengden mat du spiser.
Appetittdemping: GLP-1 demper også appetitten ved å virke på metthetssenteret i hjernen, noe som igjen reduserer mengden mat som spises. Dette er den viktigste mekanismen i vekttapsbehandling.
Regulering av blodsukkernivået: GLP-1 er svært effektivt når det gjelder å regulere blodsukkeret, særlig ved å øke insulinsekresjonen og redusere glukagonsekresjonen, og bidrar dermed til å kontrollere det postprandiale blodsukkeret.
Forbedring av fettmetabolismen: GLP-1 har også vist seg å bidra til fettforbrenning og kan spille en aktiv rolle i vekttap.
Bruk av GLP-1-baserte legemidler:
På grunn av de mange fordelene har GLP-1-baserte legemidler blitt brukt til å behandle type 2-diabetes og fedme. Disse legemidlene etterligner ofte effekten av GLP-1 for å øke insulinsekresjonen, redusere appetitten og akselerere fettmetabolismen.
Vanlige GLP-1-legemidler inkluderer:
Liraglutid, som Saxenda (for vekttap) og Victoza (for diabetesbehandling).
Dulaglutid, for eksempel Trulicity.
Semaglutid, f.eks. Ozempic og Wegovy, en GLP-1-reseptoragonist som har vært mye brukt de siste årene for vekttap og diabetesbehandling.
GLP-1 og vekttap:
GLP-1-klassen av legemidler har vist seg å ha betydelig effekt på vekttap, særlig hos pasienter med fedme og type 2-diabetes. Disse legemidlene hjelper pasientene med å redusere kaloriinntaket på en naturlig måte ved å redusere appetitten og forsinke magesekktømmingen, noe som resulterer i et sunt vekttap.
Bivirkninger av GLP-1:
Selv om GLP-1-legemidler har mange fordeler, kan de også forårsake en rekke bivirkninger, spesielt i de tidlige stadiene av behandlingen. Vanlige bivirkninger inkluderer:
Kvalme og oppkast (spesielt i starten)
Diaré eller forstoppelse
Mageproblemer
Lavt blodsukker (spesielt når det brukes i kombinasjon med andre hypoglykemiske midler)
GLP-1-analoger har vist seg å være svært effektive i behandlingen av type 2-diabetes og ved vektreduksjon, men bruken av dem må overvåkes av lege for å sikre at de er trygge og effektive.

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