Midsummer health, avoid these mistakes!

In the middle of summer in June, the weather became hotter, coupled with the increasing rain, hot and humid weather appeared in most parts of the country, easy to make people feel tired limbs, listless and sleepy, the sense of discomfort greatly increased.

Some sugar friends in the summer, often appear dizzy distension, fatigue, meat pain, heavy limbs, tiredness and lethargy, chest sulky short, even low fever does not retreat, accompanied by tasteless, poor appetite and other uncomfortable symptoms, this is often said by people “bitter summer”.
In addition, because climate change will bring a series of problems, whether for health maintenance or disease control, may have a negative impact.

Grain in Ear before and after, what health mistakes are worth the majority of sugar friends alert it?
Famous sugar diabetes health education that we should pay attention to the following points.

First, poor appetite, easy to hypoglycemia

Affected by the “bitter summer” and the high temperature, many sugar friends will have a poor appetite, diet may reduce the situation.
But in summer, when the body’s metabolism is more active and the need for energy is greater, sugar lovers are more likely to suffer from low blood sugar.
How do you avoid it?

  1. Adjust your diet

Recuperate in food respect, food wants less greasy, notice light, qualitative soft, digestible.
Eating more fresh vegetables and fruits, such as tomatoes, cucumbers, bitter gourds, winter gourds, loofah and so on, can not only meet the required nutrition, but also can prevent heat stroke.

Diabetes health education of sugar masters
Sugar friends can also eat more food, such as coix seed, red beans, white lentils, wax gourd skin and so on, to prevent the evil of heat and humidity from harming the human body.

  1. Monitor blood sugar frequently

Summer blood glucose measurement should be more frequent, in order to timely understand the changes in blood glucose.
Some sugar friends often have nocturnal hypoglycemia. You might as well measure your blood sugar before going to bed. If it is lower than 5.6mmol/ L, you can eat a proper amount of food, such as cookies, milk, etc.

In order to protect your health, it is best to consult your doctor and follow your doctor’s instructions if you need to adjust your medication.

Two, excessive greed cool, easy to get sick

Summer is hot, many sugar friends like cool, especially some overweight, obese diabetes patients.
But too greedy cool is actually harmful to health, especially these mistakes, must be avoided.

1, avoid excessive air conditioning

Some sugar friends are used to staying in an air-conditioned room for a long time to enjoy the cool.
However, this may lead to their symptoms of decreased cold tolerance, and some patients may also experience significant elevated blood sugar due to lack of body heat.
This is also very easy to induce “air sickness”.
Once the immunity decreases, it will affect the control of the disease.

Diabetes health education of sugar masters
In summer, it is recommended that sugar friends do not stay in air-conditioned rooms for too long. The air conditioning temperature should be maintained at more than 26 ° C. Remember to ventilate every one or two hours.

2, avoid cold bath

When summer is hot, many people like to shower directly in cold water.
But when the skin comes into contact with cold water, the blood vessels constrict sharply, and a lot of blood rushes back to the viscera, causing the already high blood pressure to rise again.
Serious can cause cerebrovascular rupture, bleeding, stroke, coma and even death.

The healthy thing to do is to bathe in warm water.
Warm water keeps your skin clean and cool, and helps to cool down the heat and prevent illness.

  1. Avoid drinking lots of cold drinks

Sugar friends are used to eating cold drinks to cool off, which is not correct.
First of all, raw and cold food is easy to cause gastrointestinal dysfunction, diarrhea and other problems, great harm to sugar friends.

Diabetes health education of sugar masters
Secondly, some common cool drinks, such as ice cream, ice cream and so on, most of them contain a lot of sugar, sugar friends are not suitable to drink.

Finally, cold beer should never be drunk too much.
Because beer is known as “liquid bread”, said the heat is quite high, not conducive to sugar friends to protect health.

Third, too little sleep, blood sugar instability

Don’t stay up late

Before and after Grain in Ear, the day is long and the night is short. Many sugar friends get busy late at night and unconsciously start to stay up late.
This can easily lead to lack of sleep and psychological stress.
This stimulates the cerebral cortex and activates it.
Furthermore, the sympathetic nerve center of the hypothalamus is excited and the secretion of catecholamine increases, which can lead to the increase of glucagon content in the blood and inhibit the secretion of insulin, thus causing the increase of blood sugar.

Therefore, even in summer, sugar friends should also work and rest regularly, can not sleep too late, more can not get up too late, affecting the normal rhythm of sugar control.

The mechanism of anti-inflammatory action in human skin was found

Tiger ear grass () also known as stone lotus leaf, gold thread hanging lotus, tiger ear, etc., widely distributed in China.
In Japan, tiger ear grass is used as a herbal remedy for wounds and swelling, as well as as an ingredient in food and cosmetics.
Pharmacological studies showed that the extracts of Herba paniculata had antioxidant and anti-tumor activities.
However, little is known about its physiological effects on skin keratinocytes.
Its anti-inflammatory effects on the skin have not been fully explored.
In a new study published recently in the Journal of Ethnopharmacology, researchers from the Institute of Agricultural Research at Shinshu University in Japan have found that the plant can be used to treat routine infectious dermatitis.
Bacteria-specific antibiotics and anti-inflammatory steroids are commonly used to control dermatitis, but the emergence of drug-resistant bacteria and the side effects of long-term use make them less effective.
Auricularia provides a means of locally controlling inflammation in the body by stimulating a limited immune response.
Known as “Yukinoshita” in Japanese, which means “under the snow,” tiger’s ear is a highly safe plant with a proven track record of use.
It has been used for centuries in food and cosmetics, as well as medicine.
Although its anti-inflammatory effects are well known, the detailed mechanism of action has not been elucidated.
In this study, we identified a novel biological mechanism by which Auricularia auriculata extract inhibits Toll-like receptor 2 (TLR2) expression in human skin keratinocytes and TLR2-mediated inflammation.
This study provides important insights into the anti-inflammatory effects of C. paniculata in human skin.

Based on the results of this study, researchers are planning a trial of the efficacy in patients with mild acne.
This method works by a different mechanism than traditional anti-inflammatory drugs, and if the trial is successful, it is expected that the plant could be widely used as an anti-inflammatory plant.

When AIDS meets novel coronavirus, the patient will become a mutated virus incubator?

As less affluent countries around the world scramble to get the vaccine and fight the disease, researchers in South Africa have just made a worrying discovery: AIDS could exacerbate the disease.

Geneticists and infectious disease experts have identified a potentially dangerous novel coronavirus mutation in a 36-year-old South African woman, the Los Angeles Times reported.
Eight months ago, the woman was infected with Novel Coronavirus.
She was also previously infected with HIV.
The researchers said the mutation in the novel coronavirus in the woman may have been caused by the failure of her HIV treatment and impaired immune response.

Prior to the South African woman, there was little evidence that people infected with HIV might complicate the trajectory of COVID-19.
It is understood that HIV positive patients are not likely to be infected with novel coronavirus.
But Tulio de Oliveira, a geneticist at the University of KwaZulu-Natal in Durban, said the case of the South African woman showed that AIDS patients could “become the world’s factory for novel coronavirus variants.”

It is reported that there are nearly 10 million people living with HIV worldwide.
If they are also infected with a novel coronavirus, their immune system is damaged by HIV, which is likely to cause a mutation of the novel coronavirus.
This has raised concerns that AIDS could complicate efforts to eradicate COVID-19.
In less than a year and a half, COVID-19 has killed more than 3.5 million people.

Jonathan Li, an infectious disease specialist at Brigham and Women’s Hospital in Boston, was one of the first doctors to document a major novel coronavirus mutation in an immunologically compromised patient who died more than five months after being infected.
That led doctors to realize that patients like him could be powerful incubators of novel coronavirus variants.

Jonathan Lee’s largest group of patients are those with AIDS.
From the moment a potentially dangerous novel coronavirus mutation was found in AIDS patients, he said, he prayed that HIV-infected people would not be the source of mutations that could make the novel coronavirus variant more infectious or harder to prevent and treat.

It is unclear whether the Novel Coronavirus mutation carried by the South African woman is contagious.
But researchers say it may not be a coincidence that a dangerous new strain of the virus is emerging in a population like South Africa’s KwaZulu-Natal province, where more than a quarter of adults are infected with HIV.

South Africa has nearly 2.2 million untreated people living with HIV, but as of May 31, only 183,000 people had been vaccinated, prompting health authorities to fear a new outbreak.

India is currently the worst hit country in the world by COVID-19, with nearly 1 million people living with HIV not receiving treatment.
Only 12% of Indians have been vaccinated against COVID-19, while 3.2% have been fully vaccinated.

Harvard Medical School confirmed that obesity suppresses immune cells and accelerates tumor growth

In today’s society, with the development of economy and the improvement of living standard, obesity has become a major public health problem all over the world.
According to the World Health Organization (WHO), nearly 2 billion people around the world are overweight or obese, and the global obesity rate nearly tripled from 1975 to 2016, causing 2.8 million deaths each year.
In fact, obesity is not only a feature, but also a disease. People with obesity are not only inconvenient to live, but also more prone to metabolic diseases and cardiovascular and cerebrovascular diseases. In addition, many studies have shown that obesity is associated with increased risk of more than ten kinds of cancer and reduced prognosis and survival rate.
Although China is not the country with the highest percentage of obese people, it has become the world’s most obese country in recent years due to its large population base.
For years, scientists have established that metabolic changes and chronic inflammation caused by obesity drive tumor growth, but the interaction between obesity and cancer has remained elusive.
On December 9, 2020, researchers from Harvard Medical School and other institutions published a paper in the international leading academic journal Cell entitled:
Obesity Shapes Metabolism in the Tumor Microenvironment to Suppress anti-tumor Immunity. Abstract: Obesity affects the Metabolism of Tumor Microenvironment, thereby inhibiting anti-tumor Immunity.
The study showed that obesity reduced the number and antitumor activity of CD8+T cells, an important immune cell in tumors.
This is because cancer cells reprogram their metabolism in response to the increase in fat, making them better able to gobble up energy-rich fat molecules, depriving T cells of their energy supply and accelerating tumor growth.
More importantly, the research team discovered a protein called PHD3, which can inhibit excessive fat metabolism, and overexpression of PHD3 can effectively reverse the inhibition of tumor immune cells caused by high-fat diet, which is expected to become a new target for cancer treatment.
Definition of obesity
BMI, also known as body mass index, is a commonly used international standard to measure the degree of fat and health of a person.
BMI = weight (Kg) divided by height squared (m2). A BMI greater than 25 is considered overweight, while a BMI greater than 30 is considered obese.
Obesity leads to an undersupply of energy for T cells in tumors
To reveal the effect of obesity on cancer, the team studied mouse models with different cancer types, showing that a high-fat diet leads to obesity in mice, and that high-fat diet-induced obesity damages CD8+T cells in the tumor microenvironment and accelerates tumor growth.
Further experiments showed that diet-related differences in tumor growth were particularly dependent on CD8+T cell activity.
If CD8+T cells were eliminated experimentally in mice, diet did not affect the rate of tumor growth.
Surprisingly, the high-fat diet reduced the presence of CD8+T cells in the tumor microenvironment without reducing CD8+T cells in other parts of the body.
The remaining CD8+T cells in tumors are less robust, divide more slowly, and show signs of reduced activity.
But when the cells were isolated and grown under laboratory conditions, they showed normal activity, suggesting that something in the tumor was impelling the CD8+T cells.
Specifically, on a high-fat diet, cancer cells are able to reprogram their metabolism to increase fat uptake and use, while CD8+T cells are unable to, ultimately resulting in the depletion of certain fatty acids in the tumor microenvironment, rendering CD8+T cells unable to obtain this essential energy source.
“The abnormal consumption of fatty acids is one of the most surprising findings of this study,” said Alison E. Ringel, the study’s lead author. “It shows that obesity can change the way different cells in a tumor use their energy sources, which is both surprising and exciting.”
Identify potential therapeutic targets
Next, the team identified diet-related changes in metabolic pathways in tumor cells and immune cells in the tumor microenvironment using several different methods, including single-cell gene expression analysis, large-scale protein analysis, and high-resolution imaging.
Of particular interest in these metabolic changes was PHD3, which inhibits excessive fatty acid metabolism in normal cells, while the team found that PHD3 expression was significantly reduced in cancer cells in an obese environment.
The team overexpressed PHD3 in cancer cells, resulting in a decrease in the ability of the tumor cells in obese mice to metabolize fat, an increase in free fatty acids in the tumor microenvironment, and, more importantly, a recovery in the number of CD8+T cells in the tumor.
The cyan is tumor tissue and the red is CD8+T cells
Overall, the study found and confirmed that obesity reduces the number and antitumor activity of an important immune cell called CD8+T cells within tumors.
This is because cancer cells reprogram their metabolism in response to the increase in fat, making them better able to gobble up energy-rich fat molecules, depriving T cells of their energy supply and accelerating tumor growth.
More importantly, the research team discovered a protein called PHD3, which can inhibit excessive fat metabolism, and overexpression of PHD3 can effectively reverse the inhibition of tumor immune cells caused by high-fat diet, which is expected to become a new target for cancer treatment.
In recent years, the development of cancer immunotherapy is greatly affecting the lives of cancer patients. However, cancer immunotherapy does not benefit everyone.
The study suggests that there is a metabolic tug of war between T cells and tumor cells, and who is dominant changes with obesity.
This could help scientists start thinking about cancer immunotherapies and combination therapies.
These results also lay the foundation for a better understanding of how obesity affects cancer and how a patient’s metabolism affects treatment outcomes.

How does children complement vitamin scientifically?Should I take vitamin supplements?

Vitamins are one
The body needs for nutrition and growth
Organic compounds,
Is the human body conditioning function
And normal metabolic processes
Essential substance.

Now there are more and more parents
The awareness of vitamins continues to improve,
Always worrying about the kids
Lack of various vitamins,
Always give your baby
Oral vitamin supplements,
Does this make sense?
On this Children’s Day,

Pediatric expert of the first hospital of China Medical University
Tell you about it.
First, we need to know that there are two types of vitamins: fat-soluble vitamins and water-soluble vitamins.
Among them, fat soluble vitamins mainly include vitamin A(carotene), D, E, K, etc. 4, water soluble vitamins mainly include B vitamins (vitamins B1, B2, B3, B5, B6, B11, B12, choline, vitamin H) and vitamin C, etc. 10.

The Fat-soluble vitamins are stored in the liver and are not easily excreted, so if you take too much of them, you can get toxic.
Unlike the water-soluble vitamins, there are fewer of them in the body and most of them are excreted in the urine, so they are almost non-toxic and are less likely to cause poisoning if consumed in high doses.
So when we supplement fat soluble vitamins, we must be alert to the toxic phenomenon caused by drug overdose!

Most vitamins are
You can get it through your diet.

So,
If you are deficient in vitamins,
What diseases do they cause?
How do we add to that?
From what foods do you get it?

Vitamin A
It has the function of maintaining vision and promoting growth and development.
Vitamin A deficiency, which causes what’s known as night blindness, dry eyes, dry skin and hair follicle papules, can also cause developmental disorders in children, recurrent respiratory infections, diarrhoea and anemia.
Vitamin A deficiency usually does not occur if animal foods rich in vitamin A (such as milk, eggs, liver, etc.) or dark green vegetables or yellow-red fruits are regularly consumed in our daily life. Therefore, oral vitamin A supplements are not normally required for children.

Vitamin D
It has the function of promoting calcium absorption and helping bone formation.
Rickets of vitamin Ddeficiency is a familiar disease to parents, mainly in infants and young children.
With the continuous science popularization of health education, people’s cognition of vitamin D is constantly improving, and parents are also paying more and more attention to vitamin D supplement.
However, we may have overlooked one of the simplest, effective and economical ways to get vitamin D, that is, “sun exposure”. As long as you make sure to bathe in the sun for 1-2 hours a day, you can get enough vitamin D with comfort and no damage to your skin.
For infants, breastfeeding, outdoor activities, 1-2 hours a day, and vitamin D400IU from the first 2 weeks after birth to the age of 2 years should be advocated. Additional vitamin D supplementation is not necessary if infants take more than 500ml formula milk daily (providing 200IU of vitamin D), together with appropriate outdoor activities.
For premature infants, low birth weight infants and twins with multiple fetuses, vitamin D800-1000IU/d should be given immediately after birth, and 400IU/d after 3 months to 2 years of age.
In clinical work, we often find that some infants will appear such as hyperhidrosis, night terrors, night crow, irritability, and occult alopecia, which is the initial manifestation of vitamin D deficiency. At this time, oral vitamin D1000-2000IU/ D is required, and it is changed to 400IU/ D after 1 month.
If the skeletal system changes such as “square skull, late eething, chicken breast, O-leg and X-leg” begin to appear, then this is the extreme stage of vitamin D deficiency. Combined with the laboratory indicators, oral vitamin D3000-4000IU/ D should be taken in the middle stage, and 5000-6000IU/ D should be taken in the severe stage. After 1 month, it should be changed to 400IU/ D.
In fact, in clinical work will find that many parents give their babies vitamin D supplements, but why also appear above symptoms?
There are many reasons for this, and the most common one is that the supplement dose is insufficient. Therefore, in this case, we should go to the hospital in time to test the blood 25- (OH) -D and give adequate treatment.

So,
Is it after 2
You don’t need vitamin D?
Of course not!

When children are growing faster, do not get outdoors and do not get enough sunlight, they should be given oral doses of vitamin D depending on their symptoms and test results.

Vitamin E
It has the function of delaying cell senescence, desalinating scar, diuresis and lowering blood pressure, preventing premature birth and abortion.
Vitamin E deficiency in infants, especially premature infants, often leads to brain dysfunction and retinopathy.
Daily diet such as vegetable oil, oily seeds and malt, nuts and egg yolk are rich in vitamin E, so the general children are not easy to lack, but the activity of vitamin E is significantly reduced when frying, try to let the baby away from fried food!
Vitamin K
It has a coagulant effect.
Vitamin K deficiency can cause natural bleeding, intracranial bleeding.
There are no bacteria in the intestines of newborns after birth, so newborns may suffer from vitamin K deficiency. Usually pregnant women need to inject vitamin K and give their newborns vitamin K1 supplements. 1-5mg a day can prevent neonatal vitamin K deficiency.
Foods, especially green vegetables, contain vitamin K, as do animal liver and soy.
Vitamin B1
It has the function of promoting carbohydrate metabolism, protecting nervous system and skeletal muscle system, enhancing appetite and healthy development of human body.
Beriberi is a systemic disease caused by long-term deficiency of vitamin B1 (also known as thiamine) in the body. Clinically, it is characterized by symptoms of the nervous system, cardiovascular system and gastrointestinal tract, which is more common in areas where white rice is the staple food.
Children in the daily diet to ensure that eggs, milk and meat and other vitamin B1 rich food intake can be prevented.
Vitamin B2
That is, riboflavin, vitamin B2 deficiency, also known as riboflavin deficiency, with tongue, lip, mouth, external genitalia and other skin mucosal lesions are characterized, such as keratitis, lip inflammation, glossitis, vasoproliferative conjunctivitis, seborrheic dermatitis.
What food contains rich vitamin B2?
Animal liver, kidney, heart, egg yolk, milk, beans and green leafy vegetables contain more vitamin B2 than roots and cucumbers and eggplants, which shows how important a balanced diet for children is!
  
Vitamin B6
It has the function of regulating nerve and participating in the formation of antibodies.
Vitamin B6 deficiency is mainly manifested as refractory convulsions, peripheral neuritis, dermatitis and small cell anemia.
The best source of daily vitamin B6 supplement is animal food such as butter, eggs, liver and other animal offal;
Banana, persimmon, orange, peach and other fruits contain a relatively rich amount.
Vitamin B12
Cobalamin, also known as cobalamin, prevents anemia, improves the nervous system, enhances memory and balance.
Children can obtain vitamin B12 from foods containing animal liver, kidney, beef, pork, chicken, fish, clams, eggs, milk, cheese, dairy products, fermented bean curd, etc.
 
Vitamin C
It can accelerate wound healing, especially scald and knife wounds, and help to absorb iron. It can also lower cholesterol, prevent bacterial infection, stop diarrhea and cure colds.
Scurvy is a peripheral disease characterized by extensive bleeding of the gums, skin and even the whole body caused by chronic vitamin C deficiency.
Vitamin C is not normally synthesized by the body and can be obtained from the diet of citrus fruits, green leafy vegetables, unprocessed meat, breast milk and milk.
  
Folic acid
Also known as vitamin B9, vitamin M, vitamin BC.
Folate deficiency is mainly manifested by megaloblastic anemia, but also accompanied by irritability, long-term diarrhea, growth retardation and other symptoms.
Folic acid is found in all foods that contain vitamin C, such as fresh vegetables and fruits, so it is usually not necessary to take supplements.
Folic acid supplementation is not necessary if the diet is comprehensive and rich in animal and plant protein and various vitamins and inorganic salts (such as calcium, iron, zinc, etc.).
It is worth mentioning that kiwi fruit contains up to 8% folic acid, a natural folic acid reputation, often eat to help prevent fetal birth defects and congenital heart disease.
 

To sum up,
If children in daily life
Being able to eat a balanced diet,
So most vitamins
There will be no shortage of phenomena,
There is no need for oral supplements.
Of course,
Parents need to remember
Vitamin D is an exception,
It needs to
Rely on light and supplements.

The story of insulin: commemorating one hundred years of insulin discovery

Life Science
In marking the centenary of the discovery of insulin, we wanted to share some of the stories of researchers and clinicians whose pioneering work has advanced our understanding of insulin, islet biology, insulin resistance and diabetes.
Over the past century, the pursuit of “hormones of hormones” and the advancement of diabetes treatment has been filled with stories of cooperation, persistence, and triumph.
Cell Metabolism is one of the most widely used research journals in the world. It is the first time insulin has ever been discovered and the future of insulin is still promising.
Insulin: One of the greatest medical discoveries of all time
Guest Editor Tony K.T. Lam
If Tom Brady has cemented his place in the National Football League by making 10 Super Bowls in the past 30 years and winning his seventh individual Super Bowl,
The discovery of insulin 100 years ago in the physiology department of the University of Toronto is undoubtedly one of the greatest medical studies (if not just one) in history.
Just at the University of Toronto in 1921, Banting, Best, Collip, and MacLeod succeeded in extracting and purifying insulin, which was injected to lower blood sugar levels in diabetic dogs.
Soon after, researchers found that insulin injections lowered blood sugar levels in people with type 1 diabetes.
Needless to say, insulin is consistent and reproducible in lowering blood sugar levels in all species, male and female, regardless of whether they have type 1 diabetes, and it is also applicable to all species with type 2 diabetes.
After graduating as an undergraduate in 1998, I began studying the role of insulin in muscle and liver under the direction of Drs. Amira Klip and Adria Giacca in the Department of Physiology at the University of Toronto.
My research was funded with summer and postgraduate fellowships from the Banting and Best Diabetes Centre.
Adria was a postdoctoral fellow with the late Dr. Mladen Vranic, who was the last postdoctoral fellow at Dr. Best.
Over the past 40 years, in collaboration with Dr. Gary Lewis, now director of the Banting and Best Diabetes Center, and Amira, they have diligently studied how insulin affects glucose uptake in muscle and fat, as well as glucose production in cells, rats, mice, dogs, and humans.
Then I went to New York City to do postdoctoral research with Dr. Luciano Rossetti, exploring the role of insulin in the brain, and I began to meet scientists around the world, including Dr. Barbara Kahn, who, with Amira, had spent the past 40 years at Harvard studying the role of insulin in fat and muscle.
In 2006, I returned to the Toronto General Hospital Research Institute to set up my own lab.
It was there that I met Gary and other dedicated researchers, such as Drs. Bernie Zinman, Dan Drucker, and Pat Brubaker, who had explored the role of insulin and GLP-1 in cells, rodents, and humans, and whose findings, along with many other studies around the world,
It’s a field that has grown tremendously over the last 40 or 50 years.
To mark the 100th anniversary of the discovery of insulin, I have collaborated with the editors of Cell Metabolism to produce this special issue.
In addition to reviews and opinion articles, this special issue presents a timeline on the history of insulin and diabetes.
In addition, we share the personal stories of 18 scientists in the field who review the significance of insulin discovery and offer their views on the future of insulin research.
These reviews and research articles, written by dedicated women and men, mark 40 or 50 years of research into the role and secretion of insulin. Even if today’s readers can peruse these articles in detail, the impact of insulin’s discovery 100 years ago on the human body is beyond simple description.
The success of insulin in treating diabetes is beyond doubt.
In terms of my personal experience, found that insulin had a profound impact in the 100 years later, the university of Toronto team valuable legacy by banting and best diabetes center funded empowerment and plan recognition, many researchers all over the world to advance wave upon wave for the study of insulin and diabetes has dedicated his life, made great contribution to science existing understanding…
In my opinion, these are solid proof that the discovery of insulin is the GOAT of medical research.
One final point: While my story is unique to me, with 100 years of history as witness, my experience in Toronto is not unique.
I’m pretty sure that if you simply ask former postdocs and/or graduate students in Drucker’s lab in Toronto, they can more or less describe a similar rich experience.
As Roundup, Voices and Original Research articles in this issue note, we as researchers in the field of diabetes, obesity and metabolism have a lot to learn in the next 100 years.
Maybe history will repeat itself and another GOAT will appear in this field.
Time will tell what Tom Brady’s legacy will be 100 years from now.
Jesse Roth
Director of the Diabetes Research Laboratory at Northwell Medical Center
Expect to celebrate insulin
In the early 19th century, a wide range of endocrine-like systems was gradually discovered, paving the way for the discovery by Minkowski and von Mehring of the mechanism by which pancreatectomy produces hyperglycemia.
The pancreas, implanted in the abdomen and elsewhere, successfully controls blood sugar, mimicking an endogenous endocrine biological system.
For the next three decades, teams of researchers in Europe and North America worked fairly close to success in their quest to extract bioactive peptides from the pancreas.
Banting and Best, using Macleod’s formula and machinery at the University of Toronto, succeeded in producing extracts that are active in animals, but not in humans.
Another team at the University of Toronto, led by Kripp (who works in McLeod’s lab), was the first to successfully produce insulin on a large scale that can be safely used in patients with hyperglycemia.
In partnership with the pharmaceutical company Eli Lilly, they have scaled up production to meet worldwide demand.
The medical community rushed to conclude that Type 1 diabetes was under control and treatable.
In the decades that followed, the diabetes research community came to realize that insulin replacement therapy could not prevent blindness, kidney failure and shortened life in many people with type 1 diabetes, who were insulin-deficient.
The festivities celebrating the discovery of insulin in Toronto 50 and 25 years ago were limited because existing treatments for Type 1 diabetes were not yet able to prevent the disease’s devastating effects.
Today, blood sugar monitors, insulin pumps, retinal laser therapy and other treatments finally offer patients a promising path to a full, fruitful life.
But there is a great irony: the ongoing COVID-19 pandemic is killing patients and caregivers around the world, preventing us from celebrating the 100th anniversary of insulin with a sense of comfort.
Nevertheless, let’s look forward to the opportunity to celebrate the challenge of COVID-19 in the near future, so that we can sincerely and appropriately celebrate the conquest of Type 1 diabetes.
Sonia M. Najjar
Ohio University
A journey of scientific discovery of the role of insulin in lipogenesis
If we look at the before-and-after photos of the first insulin patients, there are a number of striking features. The most striking is that they were very thin before the treatment, but after the treatment they became what we would call “dramatically overweight.”
The relationship between insulin and adipogenesis remains a puzzle.
Together with other scientists, I have been trying to map the role of insulin in regulating hepatic steatosis.
We soon learned that after docking with the plasma membrane of a hepatocyte via its receptor, the insulin/receptor complex is chaperonated by CEACAM1 and enters the degradation pathway for clearance.
During this process, CeACAM1 detaches from the complex and binds to fatty acid synthase (FASN) to inhibit its activity and limit new fat generation.
These activities are closely related to the impulsive release of insulin in the portal vein, so physiological portal hyperinsulinemia will induce the expressions of CEACAM1 and FASN in liver cells, while the acute impulsive release of insulin will cause the phosphorylation of CEACAM1, which is necessary to mediate insulin clearance and inhibit FASN activity.
In recent years, hepatic steatosis has been increasingly identified as a mechanism for the development of chronic liver disease, and its association with hyperinsulinemia/insulin resistance has been questioned, and our findings contribute to the discussion.
These observations were first published in Cell Metabolism in 2005, and this was the first manuscript in the journal.
However, we cannot say for sure that this work will lead to a way to balance lipogenesis and glucose production in the liver, or whether insulin resistance is the same as insulin’s inability to inhibit lipogenesis and glucose production in the liver.
Takashi Kadowaki
Tiger Gate Hospital, Tokyo, Japan
Another 100-year harvest in insulin research
One of the most fulfilling moments in my medical career was witnessing a type 1 diabetic recover, like a miracle, from high blood sugar, excessive weight loss, and general weakness with just a single injection of insulin.
Similarly, in the nearly 100 years since its discovery, insulin has saved tens of millions of lives worldwide.
Study of insulin targets initially limited to skeletal muscle, liver, and fat cells, but now has extended to islet B cells, brain and blood vessels, and the recent research of macrophages and gut, so people bosom expectation, hope for the further study of the various organs to uncover the mysteries of these pathways in the end.
Enteroglycin or adiponectin – adiponectin receptor (Adipor) is just one example of many endocrine and nervous systems that are involved in the fine regulation of the insulin-insulin receptor (IR) system.
Insulin is appropriately called the “hormone of hormones,” and the insulin-IR system, which is regulated by upstream neural networks and peripheral organ systems, can be likened to the “chief orchestra” rather than the “conductor,” coordinating the complex mechanisms that maintain the body’s homeostasis.
In my opinion, the whole significance of insulin research is that IR in multiple organs not only holds the key to metabolic regulation, including glucose, fatty acid, ketone body and amino acid metabolism regulation, but also plays a central role in the regulation of complex inter-organ interactions.
There is no doubt that insulin research will prove to be a more fruitful and exciting field than it has been for the past 100 years, and its fruitful results will yield valuable insights into human health and disease and its mechanisms.
Michael P. Czech
Silvia Corvera
University of Massachusetts Medical School
I feel privileged to study insulin
The upsurge of research on insulin and its effects occurred during the period from 1975 to 1985.
During this period, knowledge expanded from measuring insulin’s binding to its mysterious membrane receptor to its cDNA cloning — narrowing the vast research gap.
In the midst of this mania, on a bright afternoon in 1978, Paul Pilch of the Czech Laboratory at Brown University held up an autoradiography photograph of his experiment – and we were delighted to see a single, distinct dark band appear against a perfectly clear background.
Over the next two years, Joan Massague, Paul, and the rest of our group used this technique to correctly infer the isotetramer subunit structure of the insulin receptor and to obtain a similar structure of the IGF1 receptor.
We published a paper in 1980 in PNAS that named two receptor subunits A and B, a designation that has persisted to the present day.
This is an exciting and exciting finding that has put a smile on the faces of all the researchers who were involved in the study 40 years ago.
I deeply feel, as a scientist is how honored ah!
Despite many successes like this in hundreds of laboratories, the need to translate basic research findings into clinical applications for diabetes has never been greater.
Combining powerful technologies through research efforts is our goal now.
We are combining the Corvera lab’s technology to generate large numbers of human adipose tissue stem cells with the CRISPR-based approach from the Czech lab to further enhance the therapeutic potential of insulin.
The question we wanted to explore was: can metabolic diseases be treated by cell therapy?
We recently showed that inserting a CRISPR-enhanced “hyperpowered” human fat cells into mice that had been genetically modified by humans lowered blood sugar more than ungenetically modified fat cells.
Indeed, being a scientist makes me feel honored!

Barbara E. Corkey
Boston University School of Medicine
The saga of the insulin molecule continues
The 100th anniversary of the discovery of insulin, a rare molecule, is being celebrated around the world, and it will continue to challenge and inspire humanity.
I was fortunate enough to take part in the 50th anniversary commemoration in Jerusalem, and the 100th anniversary commemoration, which is being celebrated remotely during the pandemic.
There were many important milestones in the discovery of insulin and its impact over the course of 100 years, including the treatment of diabetes;
Determination of insulin structure, synthesis and analysis;
The physiology of insulin action, including receptor interactions;
And the physiological and pathophysiological roles of insulin in energy supply and storage.
By the next anniversary, we expect to build on the current frontiers of science to have a much deeper understanding of insulin’s role in several important areas :(1) obesity and related disorders, with an emphasis on the role of the brain in the development of obesity;
(2) The mechanism of fasting insulin elevation and its effect on the development of diabetes mellitus, cancer and fatty liver;
(3) the mechanism of insulin resistance and determine whether it is harmful.
Insulin is a rare molecule, perhaps unique.
For most living people, insulin may affect their health and well-being at some point in their lives, which has been linked to many common causes, including obesity, cardiovascular disease, diabetes, cancer, fatty liver and polycystic ovary syndrome.
Insulin will continue to inspire and challenge us.
Mark A. Atkinson
University of Florida
Dream of insulin
In 1921, the discovery of a way to purify insulin from an animal’s pancreas changed the course of insulin-dependent diabetes.
The treatment, while not perfect, offers hope.
Before that, children often comatose and die from diabetic ketoacidosis — more than 50 children crammed into hospital wards as grieving family members waited for their inevitable death.
In January 1922, Leonard Thompson’s groundbreaking treatment set the course for a change in the disease that would last nearly 100 years.
In fact, there have been tremendous advances in insulin therapy over the past century, in terms of delivery methods, treatment forms, and packaging.
While it is never a good thing to have insulin-dependent diabetes, now is the right time, if one is destined to develop the disease, and for many (but not all) sufferers, the future holds promise.
Unfortunately, due to the obstacles, such as cost, insurance, government/public health policies, lack of education, the so-called pharmacy benefit managers, retail price, poor stability of insulin/lack of refrigeration equipment, etc., in the developing countries and developed countries, there are still many patients are suffering, even to death, as of 1921.
Let us pray that the dream of the inventor of insulin will be realized as soon as possible, and that it will be met for all who need it.