Plant-based diet ramps up metabolism

Plant-based participants increased after-meal calorie burn by 18.7% after 16 weeks

The study randomly assigned participants–who were overweight and had no history of diabetes–to an intervention or control group in a 1:1 ratio. For 16 weeks, participants in the intervention group followed a low-fat, plant-based diet based on fruits, vegetables, whole grains, and legumes with no calorie limit. The control group made no diet changes. Neither group changed exercise or medication routines, unless directed by their personal doctors.

#plantdiet #metabolism #diet

Hana Kahleova et al, Effect of a Low-Fat Vegan Diet on Body Weight, Insulin Sensitivity, Postprandial Metabolism, and Intramyocellular and Hepatocellular Lipid Levels in Overweight Adults, JAMA Network Open (2020). DOI: 10.1001/jamanetworkopen.2020.25454

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2773291

https://www.pcrm.org/

Green tea and Weight Loss

The analysis of 26 randomized controlled trials including 1,344 participants found that body weight and body mass index significantly changed after green tea was consumed for periods longer than 12 weeks and at a dosage of less than 800 mg/day.

Ying Lin et al, The effect of green tea supplementation on obesity: A systematic review and dose–response meta‐analysis of randomized controlled trials, Phytotherapy Research (2020). DOI: 10.1002/ptr.6697

Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Glutamine could help people with obesity reduce fat mass and inflammation

Lower glutamine-levels were also associated with larger fat cell size and higher body fat percentage independently of body-mass index (BMI), according to the study.

#glutamine #leanmass #inflammation

”Glutamine links obesity to inflammation in human white adipose tissue,” Paul Petrus, Simon Lecoutre, Lucile Dollet, Clotilde Wiel, André Sulen, Hui Gao, Beatriz Tavira, Jurga Laurencikiene, Olav Rooyackers, Antonio Checa, Iyadh Douagi, Craig E. Wheelock, Peter Arner, Mark McCarthy, Martin O. Bergo, Laurienne Edgar, Robin P. Choudhury, Myriam Aouadi, Anna Krookand Mikael Rydén, Cell Metabolism, online December 19, 2019. https://doi.org/10.1016/j.cmet.2019.11.019

Bedtime protein for bigger gains? Here’s the scoop

Bedtime protein for bigger gains? Here’s the scoop

Downing a casein shake just before sleep increases muscle mass and strength gains from resistance training, without ‘making you fat’ — but is the effect any different to your regular post-workout protein supplement.

Tim Snijders, Jorn Trommelen, Imre W. K. Kouw, Andrew M. Holwerda, Lex B. Verdijk, Luc J. C. van Loon. The Impact of Pre-sleep Protein Ingestion on the Skeletal Muscle Adaptive Response to Exercise in Humans: An Update. Frontiers in Nutrition, 2019; 6 DOI: 10.3389/fnut.2019.00017

#nighttimeprotein #casein #muscle

Low copper levels linked to fatter fat cells

Low copper levels linked to fatter fat cells

Low copper levels linked to fatter fat cells

In studies of mouse cells, researchers have found that low levels of cellular copper appear to make fat cells fatter by altering how cells process their main metabolic fuels, such as fat and sugar.

Haojun Yang, Martina Ralle, Michael J. Wolfgang, Neha Dhawan, Jason L. Burkhead, Susana Rodriguez, Jack H. Kaplan, G. William Wong, Norman Haughey, Svetlana Lutsenko. Copper-dependent amino oxidase 3 governs selection of metabolic fuels in adipocytes. PLOS Biology, 2018; 16 (9): e2006519 DOI: 10.1371/journal.pbio.2006519

 

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2006519

Flaxseed Fiber Surprising benefits for Metabolism and Overall health

Flaxseed Fiber Surprising benefits for Metabolism and Overall health

 

“Our data suggest that flaxseed fiber supplementation affects host metabolism by increasing energy expenditure and reducing obesity as well as by improving glucose tolerance. Future research should be directed to understand relative contribution of the different microbes and delineate underlying mechanisms for how flaxseed fibers affect host metabolism,” the researchers wrote.
#flaxseed #metabolism #fermentable

Tulika Arora, Olga Rudenko, Kristoffer Lihme Egerod, Anna Sofie Husted, Petia Kovatcheva-Datchary, Rozita Akrami, Mette Kristensen, Thue W. Schwartz, Fredrik Bäckhed. Microbial fermentation of flaxseed fibers modulates the transcriptome of GPR41-expressing enteroendocrine cells and protects mice against diet-induced obesity. American Journal of Physiology-Endocrinology and Metabolism, 2018; DOI: 10.1152/ajpendo.00391.2018

https://www.physiology.org/doi/abs/10.1152/ajpendo.00391.2018

New research shows cottage cheese before bed supports metabolism and muscle recovery

New research shows cottage cheese before bed supports metabolism and muscle recovery

New research shows cottage cheese before bed supports metabolism and muscle recovery

Researchers found that consuming 30 grams of protein about 30 minutes before bed appears to have a positive effect on muscle quality, metabolism and overall health. And for those who have sworn off eating at night, there is no gain in body fat

Samantha M. Leyh, Brandon D. Willingham, Daniel A. Baur, Lynn B. Panton, Michael J. Ormsbee. Pre-sleep protein in casein supplement or whole-food form has no impact on resting energy expenditure or hunger in women. British Journal of Nutrition, 2018; 120 (9): 988 DOI: 10.1017/S0007114518002416

#cottagecheese #muscle #metabolism

Camu Camu may increase metabolism through the Gut Microbiome

Camu Camu may increase metabolism through the Gut Microbiome

Camu Camu may increase metabolism through the Gut Microbiome

The researchers found that camu camu improved glucose tolerance and insulin sensitivity and reduced the concentration of blood endotoxins and metabolic inflammation. “All these changes were accompanied by a reshaping of the intestinal microbiota.

Fernando F Anhê, Renato T Nachbar, Thibault V Varin, Jocelyn Trottier, Stéphanie Dudonné, Mélanie Le Barz, Perrine Feutry, Geneviève Pilon, Olivier Barbier, Yves Desjardins, Denis Roy, André Marette. Treatment with camu camu (Myrciaria dubia) prevents obesity by altering the gut microbiota and increasing energy expenditure in diet-induced obese mice. Gut, 2018; gutjnl-2017-315565 DOI: 10.1136/gutjnl-2017-315565

Wine Polyphenols could fend off bacteria that cause cavities and gum disease

Wine Polyphenols could fend off bacteria that cause cavities and gum disease

Polyphenols could fend off bacteria that cause cavities and gum disease

The researchers checked out the effect of two red wine polyphenols, as well as commercially available grape seed and red wine extracts, on bacteria that stick to teeth and gums and cause dental plaque, cavities and periodontal disease.

Inhibition of Oral Pathogens Adhesion to Human Gingival Fibroblasts by Wine Polyphenols Alone and in Combination with an Oral Probiotic. Journal of Agricultural and Food Chemistry, 2018; DOI: 10.1021/acs.jafc.7b05466

*Grape Seed Extract may help repair Micro-cavities

http://www.youtube.com/watch?v=QRHOyntGLzg

The dark side of artificial sweeteners

Contact: Mary Beth O’Leary moleary@cell.com 617-397-2802 Cell Press

More and more Americans are consuming artificial sweeteners as an alternative to sugar, but whether this translates into better health has been heavily debated. An opinion article published by Cell Press on July 10th in the journal Trends in Endocrinology & Metabolism reviews surprising evidence on the negative impact of artificial sweeteners on health, raising red flags about all sweeteners—even those that don’t have any calories.

“It is not uncommon for people to be given messages that artificially-sweetened products are healthy, will help them lose weight or will help prevent weight gain,” says author Susan E. Swithers of Purdue University. “The data to support those claims are not very strong, and although it seems like common sense that diet sodas would not be as problematic as regular sodas, common sense is not always right.”

Consumption of sugar-sweetened drinks has been linked to obesity, type 2 diabetes, and metabolic syndrome—a group of risk factors that raises the risk for heart disease and stroke. As a result, many Americans have turned to artificial sweeteners, which are hundreds of times sweeter than sugar but contain few, if any, calories. However, studies in humans have shown that consumption of artificially sweetened beverages is also associated with obesity, type 2 diabetes, and metabolic syndrome as well as cardiovascular disease. As few as one of these drinks per day is enough to significantly increase the risk for health problems.

Moreover, people who regularly consume artificial sweeteners show altered activation patterns in the brain’s pleasure centers in response to sweet taste, suggesting that these products may not satisfy the desire for sweets. Similarly, studies in mice and rats have shown that consumption of noncaloric sweeteners dampens physiological responses to sweet taste, causing the animals to overindulge in calorie-rich, sweet-tasting food and pack on extra pounds.

Taken together, the findings suggest that artificial sweeteners increase the risk for health problems to an extent similar to that of sugar and may also exacerbate the negative effects of sugar. “These studies suggest that telling people to drink diet sodas could backfire as a public health message,” Swithers says. “So the current public health message to limit the intake of sugars needs to be expanded to limit intake of all sweeteners, not just sugars.”

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Trends in Endocrinology & Metabolism, Swithers et al.: “Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.”

Carnitine supplements reverse glucose intolerance in animals

2009 study posted for filing

Contact: Mary Jane Gore
mary.gore@duke.edu
919-660-1309
Duke University Medical Center

DURHAM, N.C. – Supplementing obese rats with the nutrient carnitine helps the animals to clear the extra sugar in their blood, something they had trouble doing on their own, researchers at Duke University Medical Center report.

A team led by Deborah Muoio (Moo-ee-oo), Ph.D., of the Duke Sarah W. Stedman Nutrition and Metabolism Center, also performed tests on human muscle cells that showed supplementing with carnitine might help older people with prediabetes, diabetes, and other disorders that make glucose (sugar) metabolism difficult.

Carnitine is made in the liver and recycled by the kidney, but in some cases when this is insufficient, dietary carnitine from red meat and other animal foods can compensate for the shortfall.

After just eight weeks of supplementation with carnitine, the obese rats restored their cells’ fuel- burning capacity (which was shut down by a lack of natural carnitine) and improved their glucose tolerance, a health outcome that indicates a lower risk of diabetes.

These results offer hope for a new therapeutic option for people with glucose intolerance, older people, people with kidney disease, and those with type 2 diabetes (what used to be called adult-onset diabetes).

Muoio said that soon her team of researchers will begin a small clinical trial of carnitine supplementation in people who fit the profile of those who might benefit from additional carnitine – older people (60 to 80 years) with glucose intolerance.

The study is published in the Aug. 21 issue of the Journal of Biological Chemistry.

The Duke researchers began studying carnitine more closely when abnormalities in the nutrient emerged from blood chemistry profiles of obese and old animals. These chemical profiles report on hundreds of byproducts of cell metabolism called metabolites and give scientists an opportunity to identify markers of disease states.

Carnitine is a natural compound known for helping fatty acids enter the mitochondria, the powerhouses of cells, where fatty acids are “burned” to give cells energy for their various tasks. Carnitine also helps move excess fuel from cells into the circulating blood, which then redistributes this energy source to needier organs or to the kidneys for removal. These processes occur through the formation of acylcarnitine molecules, energy molecules that can cross membrane barriers that encase all cells.

Researchers at Duke had observed that skeletal muscle of obese rats produced high amounts of the acylcarnitines, which requires free carnitine. As these molecules started to accumulate, the availability of free, unprocessed carnitine decreased. This imbalance was linked to fuel-burning problems, that is, impairments in the cells’ combustion of both fat and glucose fuel.

“We suspected that persistent increases in acylcarnitines in the rats were causing problems, and we could also see that the availability of free carnitine was decreasing with weight gain and aging,” said Muoio. “It appeared that carnitine could no longer do its job when chronic metabolic disruptions were stressing the system. That’s when we designed an experiment to add extra carnitine to the rats’ diet.”

Muoio is also a professor in the departments of medicine, pharmacology and cancer biology.

 

###

 

Other study authors included Robert C. Noland, Sarah E. Seiler, Helen Lum, Olga Ilkayeva, Robert Stevens, and Timothy R. Koves of the Sarah W. Stedman Nutrition and Metabolism Center. Koves is also with the Duke Department of Medicine. Robert M. Lust is with the Department of Physiology at East Carolina University in Greenville, N.C., and Fausto G. Hegardt is with the CIBER division Fisiopatología de la Obesidad y la Nutrición of the Instituto de Salud Carlos III in Spain.

The work was supported by grants from the National Institutes of Health, and the American Diabetes Association, and a John A. Hartford Duke Center for Excellence Award

High Fat diets can disrupt our Biological Clock : Through the adiponectin signaling pathway

2008 study posted for filing

Contact: Jerry Barach
jerryb@savion.huji.ac.il
972-258-82904
The Hebrew University of Jerusalem

Another reason to avoid high-fat diet — it can disrupt our biological clock

Jerusalem, December 28, 2008 – Indulgence in a high-fat diet can not only lead to overweight because of excessive calorie intake, but also can affect the balance of circadian rhythms – everyone’s 24-hour biological clock, Hebrew University of Jerusalem researchers have shown.

The biological clock regulates the expression and/or activity of enzymes and hormones involved in metabolism, and disturbance of the clock can lead to such phenomena as hormone imbalance, obesity, psychological and sleep disorders and cancer.

While light is the strongest factor affecting the circadian clock, Dr. Oren Froy and his colleagues of the Institute of Biochemistry, Food Science and Nutrition at the Hebrew University’s Robert H. Smith Faculty of Agriculture, Food and Environment in Rehovot, have demonstrated in their experiments with laboratory mice that there is a cause-and-effect relation between diet and biological clock imbalance.

To examine this thesis, Froy and his colleagues, Ph.D. student Maayan Barnea and Zecharia Madar, the Karl Bach Professor of Agricultural Biochemistry, tested whether the clock controls the adiponectin signaling pathway in the liver and, if so, how fasting and a high-fat diet affect this control. Adiponectin is secreted from differentiated adipocytes (fat tissue) and is involved in glucose and lipid metabolism. It increases fatty acid oxidation and promotes insulin sensitivity, two highly important factors in maintaining proper metabolism.

The researchers fed mice either a low-fat or a high-fat diet, followed by a fasting day, then measured components of the adiponectin metabolic pathway at various levels of activity. In mice on the low-fat diet, the adiponectin signaling pathway components exhibited normal circadian rhythmicity. Fasting resulted in a phase advance. The high-fat diet resulted in a phase delay. Fasting raised and the high-fat diet reduced adenosine monophosphate-activated protein kinase (AMPK) levels. This protein is involved in fatty acid metabolism, which could be disrupted by the lower levels.

In an article soon to be published by the journal Endocrinology, the researchers suggest that this high-fat diet could contribute to obesity, not only through its high caloric content, but also by disrupting the phases and daily rhythm of clock genes. They contend also that high fat-induced changes in the clock and the adiponectin signaling pathway may help explain the disruption of other clock-controlled systems associated with metabolic disorders, such as blood pressure levels and the sleep/wake cycle

Natural compound helps reverse diabetes in mice – nicotinamide mononucleotide / NAD

Contact: Julia Evangelou Strait straitj@wustl.edu 314-286-0141 Washington University School of Medicine

Natural compound helps reverse diabetes in mice

Researchers at Washington University School of Medicine in St. Louis have restored normal blood sugar metabolism in diabetic mice using a compound the body makes naturally. The finding suggests that it may one day be possible for people to take the compound much like a daily vitamin as a way to treat or even prevent type 2 diabetes.

This naturally occurring compound is called nicotinamide mononucleotide, or NMN, and it plays a vital role in how cells use energy.

“After giving NMN, glucose tolerance goes completely back to normal in female diabetic mice,” says Shin-ichiro Imai, MD, PhD, associate professor of developmental biology. “In males, we see a milder effect compared to females, but we still see an effect. These are really remarkable results. NMN improves diabetic symptoms, at least in mice.”

The research appears online Oct. 4 in Cell Metabolism.

Imai says this discovery holds promise for people because the mechanisms that NMN influences are largely the same in mice and humans.

“But whether this mechanism is equally compromised in human patients with type 2 diabetes is something we have to check,” Imai says. “We have plans to do this in the very near future.”

All cells in the body make NMN in a chain of reactions leading to production of NAD, a vital molecule that harvests energy from nutrients and puts it into a form cells can use. Among other things, NAD activates a protein called SIRT1 that has been shown to promote healthy metabolism throughout the body, from the pancreas to the liver to muscle and fat tissue.

According to the study, aging and eating a high-fat diet reduce production of NMN, slowing the body’s production of NAD and leading to abnormal metabolic conditions such as diabetes. NAD cannot be given to the mice directly because of toxic effects. But after administering NMN, levels of NAD rise and the diabetic mice show dramatically improved responses to glucose. In some cases, they return to normal.

“I’m very excited to see these results because the effect of NMN is much bigger than other known compounds or chemicals,” says first author Jun Yoshino, MD, PhD, postdoctoral research associate. “Plus, the fact that the body naturally makes NMN is promising for translating these findings into humans.”

Imai and his colleagues found that young, healthy mice on a high-fat diet developed diabetes in six months or less. In these mice, they found that NAD levels were reduced. But after administering NMN, levels of NAD increased and the female mice had normal results in glucose tolerance tests — a measure of how well the body moves glucose from the blood to the organs and tissues for use. Glucose tolerance was also improved after male diabetic mice received NMN but did not quite return to normal. The researchers are interested in learning more about these differences between male and female mice.

“We don’t have a clear answer, but we are speculating that sex hormones, such as estrogen, may be important downstream for NAD synthesis,” Yoshino says.

In older mice, they observed that about 15 percent of healthy males fed a normal diet developed diabetes.

“When we injected these older diabetic mice with NMN, they had improved glucose tolerance, even after one injection,” says Kathryn F. Mills, research lab supervisor and an equally contributing first author of the study. “We also injected older healthy mice and found that they weren’t adversely affected. It’s good to know that even if the mice are not diabetic, giving NMN is not going to hurt them.”

Imai says few studies have examined normal mice that naturally develop diabetes as a simple result of aging because the experiments take so long. In an interesting twist, few elderly female mice developed diabetes at all. But after switching to a high fat diet, older female mice quickly developed severe diabetes.

“Again, when we injected these females with NMN, we came up with a completely normal glucose tolerance curve,” Mills says. “We can also see that the NMN has completely reversed and normalized the levels of cholesterol, triglycerides and free fatty acids.”

Though the mice received NMN by injection in this study, Imai’s group is now conducting a long-term study of diabetic mice that get NMN dissolved in their drinking water. Imai calls this work a first step toward a possible “nutriceutical” that people could take almost like a vitamin to treat or even prevent type 2 diabetes.

“Once we can get a grade of NMN that humans can take, we would really like to launch a pilot human study,” Imai says.

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Yoshino J, Mills KF, Yoon MJ, Imai SI. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism. Online Oct. 4, 2011.

This work was supported in part by the National Institute on Aging, the Ellison Medical Foundation, the Longer Life Foundation, the Washington University Nutrition Obesity Research Center, the Washington University Diabetes Research and Training Center. Jun Yoshino is supported by the Japan Research Foundation for Clinical Pharmacology, the Manpei Suzuki Diabetes Foundation, and the Kanae Foundation for the Promotion of Medical Science.

Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare