Saltar para: Posts [1], Pesquisa e Arquivos [2]

http://cyto.blogs.sapo.pt

Espaço de publicação e discussão sobre oncologia. GBM IMMUNOTHERAPY ONCO-VIRUS ONCOLOGY CANCER CHEMOTHERAPY RADIOTHERAPY


Quarta-feira, 19.08.15

Inflammation from diets deficient in nutrients contribute to weight despite intake of macronutrients

 

Inflammation from diets deficient in nutrients contribute to weight despite intake of macronutrients

Published on August 6, 2015 at 8:41 AM ·

If you are watching what you eat, working out, and still not seeing improvements in your cholesterol, blood pressure, blood sugar, etc., here's some hope. A new report appearing in the August 2015 issue of The FASEB Journal suggests that inflammation induced by deficiencies in vitamins and minerals might be the culprit. In this report, researchers show that - in some people - improvement results in many of the major markers of health when nutritional deficiencies are corrected. Some even lost weight without a change in their diet or levels of activity.

"It is well known that habitual consumption of poor diets means increased risk of future disease, but clearly this is not a compelling enough reason for many to improve their eating habits," said Bruce Ames, Ph.D., a senior scientist at Children's Hospital Oakland Research Institute, director of their Nutrition and Metabolism Center, and a professor emeritus of Biochemistry and Molecular Biology at the University of California, Berkeley. "However, a relatively easy intervention with something like the nutrient bar used in this study may help people to realize the positive impact that a diet with adequate nutrition can have in their daily lives, which may be a stronger incentive for change."

To make their Ames and colleagues undertook three clinical trials in which adults ate two nutrient bars each day for two months. Participants acted as their own controls, meaning that changes in a wide variety of biochemical (e.g., HDL-c, LDL-c, insulin) and physical (e.g., blood pressure, weight) measurements were recorded in each individual over the two-month period. People who were overweight/obese moved in a healthier metabolic direction (e.g., improved HDL, LDL, insulin, glucose, etc.), and some lost weight by just eating small, low-calorie, nutrient bars each day for two months, without any additional requirements.

"If being healthy was as simple as 'losing weight' or 'keeping thin,' our ancient ancestors who lived in times of extreme food scarcity might still be with us today," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This report shows that what you eat is as important, if not more, than how much you eat and how many calories you burn in the gym."

Source:

Federation of American Societies for Experimental Biology

Autoria e outros dados (tags, etc)

por cyto às 11:56

Quarta-feira, 19.08.15

Low-fat diets better than low-carb diets for weight loss, NIH study finds

Low-fat diets better than low-carb diets for weight loss, NIH study finds

Published on August 14, 2015 at 7:30 AM ·

In a recent study, restricting dietary fat led to body fat loss at a rate 68 percent higher than cutting the same number of carbohydrate calories when adults with obesity ate strictly controlled diets. Carb restriction lowered production of the fat-regulating hormone insulin and increased fat burning as expected, whereas fat restriction had no observed changes in insulin production or fat burning. The research was conducted at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. Results were published August 13 in Cell Metabolism.

"Compared to the reduced-fat diet, the reduced-carb diet was particularly effective at lowering insulin secretion and increasing fat burning, resulting in significant body fat loss," said Kevin Hall, Ph.D., NIDDK senior investigator and lead study author. "But interestingly, study participants lost even more body fat during the fat-restricted diet, as it resulted in a greater imbalance between the fat eaten and fat burned. These findings counter the theory that body fat loss necessarily requires decreasing insulin, thereby increasing the release of stored fat from fat tissue and increasing the amount of fat burned by the body."

The researchers studied 19 non-diabetic men and women with obesity in the Metabolic Clinical Research Unit at the NIH Clinical Center in Bethesda, Maryland. Participants stayed in the unit 24 hours per day for two extended visits, eating the same food and doing the same activities. For the first five days of each visit they ate a baseline balanced diet. Then for six days, they were fed diets containing 30 percent fewer calories, achieved by cutting either only total carbs or total fat from the baseline diet, while eating the same amount of protein. They switched diets during the second visit.

The researchers had previously simulated the study with a math model of human metabolism, whose body fat predictions matched the data later collected in the study. When simulating what might happen over longer periods, the model predicted relatively small differences in body fat loss with widely varying ratios of carbs to fat. Those results suggest the body may eventually minimize differences in body fat loss when diets have the same number of calories. More research is needed to assess the physiological effects of fat and carb reduction in the long term.

"This NIH study provides invaluable evidence on how different types of calories affect metabolism and body composition," said NIDDK Director Griffin P. Rodgers, M.D. "The more we learn about the complicated topic of weight loss, the better we can find ways to help people manage their health."

More than two-thirds of American adults are overweight or obese. Maintaining a healthy weight can help prevent complications related to overweight and obesity such as heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.

"Our data tell us that when it comes to body fat loss, not all diet calories are exactly equal," Hall said. "But the real world is more complicated than a research lab, and if you have obesity and want to lose weight, it may be more important to consider which type of diet you'll be most likely to stick to over time."

Source:

NIH/National Institute of Diabetes and Digestive and Kidney Diseases

 

Autoria e outros dados (tags, etc)

por cyto às 11:47

Sábado, 04.07.15

effect of pioglitazone and other antidiabetics on dementia

Pioglitazone drug significantly decreases risk of dementia

Published on June 23, 2015 at 2:03 PM 

Patients with type 2 diabetes have a dysfunctional sugar metabolism because the essential hormone insulin does not work effectively. Once the disease reaches an advanced stage, the body stops producing insulin altogether, which means that it has to be administered externally. Type 2 diabetes most commonly occurs in late adulthood, and it has long been known that it can affect the patient's mental health: Patients have a greater risk of developing dementia than non-diabetics. However, how does antidiabetic medication influence this risk? Neurologist Michael Heneka and the demographers Anne Fink and Gabriele Doblhammer investigated this issue in the current study. Their work is based on data from the years 2004 to 2010 provided by the German public health insurance company AOK. These data set comprises information about diseases and medication related to more than 145,000 men and women aged 60 and over.

Long-term treatment reduced dementia risk

The analysis confirmed previous findings that diabetics have an increased risk of developing dementia. However, it was also found that this risk can significantly be modified by pioglitazone. This drug is taken as tablets. It is applied in short-term as well as in long-term treatment of diabetes as long as the body is still capable of producing its own insulin.

"Treatment with pioglitazone showed a remarkable side benefit. It was able to significantly decrease the risk of dementia," says Doblhammer. "The longer the treatment, the lower the risk." Risk reduction was most noticeable when the drug was administered for at least two years. Diabetics given this treatment developed dementia less often than non-diabetics. Doblhammer: "The risk of developing dementia was around 47 percent lower than in non-diabetics, i.e. only about half as large."

Metformin - another frequently prescribed antidiabetic drug - also lowered the risk of developing dementia. However, the effect was lower than that of pioglitazone.

Protection against nerve cell damage

Pioglitazone improves the effect of the body's own insulin. Moreover, laboratory tests have long indicated that it also protects the nerve cells. The current results are therefore no surprise to neuroscientist Michael Heneka. "Pioglitazone is an anti-inflammatory drug that also inhibits the deposition of harmful proteins in the brain," he says.

However, Heneka emphasizes that the exact mechanisms are not yet understood: "Our study suggests that pioglitazone has a preventive effect. This happens when the drug is taken before symptoms of dementia manifest. Thus, it protects in particular against Alzheimer's, the most common form of dementia. The causes for this, whether pioglitazone only has this protective effect in diabetics or if it would also work in non-diabetics - all these questions have yet to be answered. The next logical step would therefore be clinical studies. These studies would specifically investigate the effect of pioglitazone and other antidiabetics on dementia."

Source:

DZNE - German Center for Neurodegenerative Diseases

Autoria e outros dados (tags, etc)

por cyto às 11:54

Sábado, 04.07.15

way to stop growth of cancer cells by targeting the Warburg Effect

SLU researchers find way to stop growth of cancer cells by targeting the Warburg Effect

Published on June 26, 2015 at 10:55 PM 

In research published in Cancer Cell, Thomas Burris, Ph.D., chair of pharmacology and physiology at Saint Louis University, has, for the first time, found a way to stop cancer cell growth by targeting the Warburg Effect, a trait of cancer cell metabolism that scientists have been eager to exploit.

Unlike recent advances in personalized medicine that focus on specific genetic mutations associated with different types of cancer, this research targets a broad principle that applies to almost every kind of cancer: its energy source.

The Saint Louis University study, which was conducted in animal models and in human tumor cells in the lab, showed that a drug developed by Burris and colleagues at Scripps Research Institute can stop cancer cells without causing damage to healthy cells or leading to other severe side effects.

The Warburg Effect

Metabolism -- the ability to use energy -- is a feature of all living things. Cancer cells aggressively ramp up this process, allowing mutated cells to grow unchecked at the expense of surrounding tissue.

"Targeting cancer metabolism has become a hot area over the past few years, though the idea is not new," Burris said.

Since the early 1900s, scientists have known that cancer cells prefer to use glucose as fuel even if they have plenty of other resources available. In fact, this is how doctors use PET (positron emission tomography) scan images to spot tumors. PET scans highlight the glucose that cancer cells have accumulated.

This preference for using glucose as fuel is called the Warburg effect, or glycolysis.

In his paper, Burris reports that the Warburg effect is the metabolic foundation of oncogenic (cancer gene) growth, tumor progression and metastasis as well as tumor resistance to treatment.

Cancer's goal: to grow and divide

Cancer cells have one goal: to grow and divide as quickly as possible. And, while there are a number of possible molecular pathways a cell could use to find food, cancer cells have a set of preferred pathways.

"In fact, they are addicted to certain pathways," Burris said. "They need tools to grow fast and that means they need to have all of the parts for new cells and they need new energy."

"Cancer cells look for metabolic pathways to find the parts to grow and divide. If they don't have the parts, they just die," said Burris. "The Warburg effect ramps up energy use in the form of glucose to make chemicals required for rapid growth and cancer cells also ramp up another process, lipogenesis, that lets them make their own fats that they need to rapidly grow."

If the Warburg effect and lipogenesis are key metabolic pathways that drive cancer progression, growth, survival, immune evasion, resistance to treatment and disease recurrence, then, Burris hypothesizes, targeting glycolysis and lipogenesis could offer a way to stop a broad range of cancers.

Cutting off the energy supply

Burris and his colleagues created a class of compounds that affect a receptor that regulates fat synthesis. The new compound, SR9243, which started as an anti-cholesterol drug candidate, turns down fat synthesis so that cells can't produce their own fat. This also impacts the Warburg pathway, turning cancer cells into more normal cells. SR9243 suppresses abnormal glucose consumption and cuts off cancer cells' energy supply.

When cancer cells don't get the parts they need to reproduce through glucose or fat, they simply die.

Because the Warburg effect is not a feature of normal cells and because most normal cells can acquire fat from outside, SR9243 only kills cancer cells and remains non-toxic to healthy cells.

The drug also has a good safety profile; it is effective without causing weight loss, liver toxicity, or inflammation.

Promising Results So far, SR9243 has been tested in cultured cancer cells and in human tumor cells grown in animal models. Because the Warburg pathway is a feature of almost every kind of cancer, researchers are testing it on a number of different cancer models.

"It works in a wide range of cancers both in culture and in human tumors developing in animal models," Burris said. "Some are more sensitive to it than others. In several of these pathways, cells had been reprogramed by cancer to support cancer cell growth. This returns the metabolism to that of more normal cells."

In human tumors grown in animal models, Burris said, "It worked very well on lung, prostate, and colorectal cancers, and it worked to a lesser degree in ovarian and pancreatic cancers."

It also seems to work on glioblastoma, an extremely difficult to treat form of brain cancer, though it isn't able to cross the brain/blood barrier very effectively. The challenge for researchers in this scenario will be to find a way to allow the drug to cross this barrier, the body's natural protection for the brain, which can make it difficult for drug treatments to reach their target.

And, in even more promising news, it appears that when SR9243 is used in combination with existing chemotherapy drugs, it increases their effectiveness, in a mechanism apart from SR9243's own cancer fighting ability.

Source:

Saint Louis University

Autoria e outros dados (tags, etc)

por cyto às 11:25


Mais sobre mim

foto do autor


Subscrever por e-mail

A subscrição é anónima e gera, no máximo, um e-mail por dia.

Pesquisar

Pesquisar no Blog  

calendário

Fevereiro 2016

D S T Q Q S S
123456
78910111213
14151617181920
21222324252627
2829