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Small rises in blood glucose trigger big changes in insulin-producing cells -- ScienceDaily

In a paper recently published in Molecular Metabolism, Weir's lab laid out a wealth of new data about how beta cells behave at slightly raised levels of blood glucose. The work provides major additional evidence of a "glucose toxicity" effect that helps to drive the development of both type 1 and type 2 diabetes. Studying beta cells in lab rats whose blood glucose levels were slightly elevated, Weir's lab found changes in gene expression that affect not just how well the cells function but their ability to divide and grow, as well as their vulnerability to autoimmunity and inflammation. Weir, professor of medicine at Harvard Medical School, has long studied a puzzling type 2 diabetes phenomenon called first-phase insulin release and how this release is shut down as the disease progresses. In healthy people with normal blood glucose levels, Weir explains, the body responds quickly to glucose with a big spike of insulin secretion. "If then you take people who have slightly higher glucose levels, above 100 mg/dl, which is still not even diabetes, this first-phase insulin release is impaired," he says. "And when the level gets above 115 mg/dl, it's gone. So virtually all the beta cells don't respond to that acute stimulus." Fortunately, the cells eventually do wake up and respond to other stimuli well enough to keep blood glucose in a prediabetic range.

Humans Roasted Starchy Carbs 170,000 Years Ago | Discover Magazine

Roasting rhizomes and other starchy plant material also makes finding evidence of them, tens of thousands of years later, much more likely. Authors of the new research note that, had the plants been eaten raw, it's unlikely any sign of them would have been preserved in the archaeological record. Something to keep in mind when you hear claims that ancient humans skipped eating starchy plants. The multiple specimens found in the ancient hearth appear to belong to the genus Hypoxis, flowering plants that include H. hemerocallidea, also known as the African potato. Researchers believe the ancient rhizomes they analyzed may belong to H. angustifolia, a species found today in much of sub-Saharan Africa and also the southern Arabian Peninsula. According to the authors, H. angustifolia would have been a reliable, year-round food source for hunter-gatherer groups moving across the ancient Southern African landscape. The rhizome provides about 120 calories per 3.5 ounces and, note the researchers, the relative ease of digging them up could have provided an entire day's caloric needs in about two hours.

Learning from the bears -- ScienceDaily

A grizzly bear only knows three seasons during the year. Its time of activity starts between March and May. Around September the bear begins to eat large quantities of food. And sometime between November and January, it falls into hibernation. From a physiological point of view, this is the strangest time of all. The bear's metabolism and heart rate drop rapidly. It excretes neither urine nor feces. The amount of nitrogen in the blood increases drastically and the bear becomes resistant to the hormone insulin.

Fatty meal interrupts gut's communication with the body, but why? If that second helping of prime rib stuns your gut into silence, is that good or bad? -- ScienceDaily

These cells produce at least 15 different hormones to send signals to the rest of the body about gut movement, feelings of fullness, digestion, nutrient absorption, insulin sensitivity and energy storage. "But they fall asleep on the job for a few hours after a high-fat meal, and we don't yet know if that's good or bad," said John Rawls, an associate professor of molecular genetics and microbiology in the Duke School of Medicine. Since enteroendocrine cells are key players in digestion, the feeling of being full and subsequent feeding behavior, this silencing may be a mechanism that somehow causes people eating a high-fat diet to eat even more. "This is a previously unappreciated part of the postprandial (after-meal) cycle," Rawls said. "If this happens every time we eat an unhealthy, high-fat meal, it might cause a change in insulin signaling, which could in turn contribute to the development of insulin resistance and Type 2 diabetes."

Refined carbs may trigger insomnia, finds study -- ScienceDaily

They found that the higher the dietary glycemic index -- particularly when fueled by the consumption of added sugars and processed grains -- the greater the risk of developing insomnia. They also discovered that women who consumed more vegetables and whole fruits (not juices) were less likely to develop insomnia. "Whole fruits contain sugar, but the fiber in them slow the rate of absorption to help prevent spikes in blood sugar," says Gangwisch. "This suggests that the dietary culprit triggering the women's insomnia was the highly processed foods that contain larger amounts of refined sugars that aren't found naturally in food." Since most people, not just postmenopausal women, experience a rapid rise in blood sugar after eating refined carbohydrates, the authors suspect that these findings may also hold true in a broader population.

Abbott Labs kills free tool that lets you own the blood-sugar data from your glucose monitor, saying it violates copyright law / Boing Boing

First, they say that creating a tool that interoperates with the Freestyle Libre's data is a copyright infringement, because the new code is a derivative work of Abbott's existing product. But code that can operate on another program's data is not a derivative work of the first program -- just because Apple's Pages can read Word docs, it doesn't mean that Pages is a derivative of MS Office. In addition, as Diabettech points out, EU copyright law explicitly contains an exemption for reverse engineering in order to create interoperability between medical devices (EU Software Directive, Article 6). More disturbing is Kirkland/Abbott's claim that the project violates Section 1201 of the Digital Millennium Copyright Act, which prohibits bypassing "access controls" for copyrighted works. Factual data (like your blood sugar levels) are not copyrightable -- and if they were, you would hold that copyright. It's your blood. What's more, DMCA 1201 also contains an interoperability exemption.

Venturing A Perspective On The Drug Pricing Debate | LifeSciVCLifeSciVC

As an example, branded insulin prices are commonly cited as having had egregious increases over time, and it’s true the list price increases have been very aggressive. But the net prices sent back to Pharma have often been very small if not negative. For a shocking image of this, check out the list-to-net price comparison of Humalog 100: $594 list price and a $135 net price after rebates. That captures the absurdity of the system. Adding insult to injury, that gross-to-net price differential isn’t passed on to consumers – it’s captured by the middleman usurpers in the healthcare system.

Short-term study suggests vegan diet can boost gut microbes related to body weight, body composition and blood sugar control -- ScienceDaily

The study included 147 participants (86% women and 14% men; mean age was 55.6±11.3 years), who were randomised to follow a low-fat vegan diet (n=73) or to make no changes to their diet (n=74) for 16 weeks. At baseline and 16 weeks, gut microbiota composition was assessed, using uBiome kits. Dual energy X-ray absorptiometry was used to measure body composition. A standard method called the PREDIM index was used to assess insulin sensitivity. Following the 16-week study, body weight was reduced significantly in the vegan group (treatment effect average -5.8 kg), particularly due to a reduction in fat mass (average -3.9 kg) and in visceral fat. Insulin sensitivity also increased significantly in the vegan group. The relative abundance of Faecalibacterium prausnitzii increased in the vegan group (treatment effect +4.8%). Relative changes in Faecalibacterium prausnitzii were associated with decreases in body weight, fat mass and visceral fat. The relative abundance of Bacteoides fragilis also increased in the vegan group (treatment effect +19.5%). Relative changes in Bacteroides fragilis were associated with decreases in body weight, fat mass and visceral fat, and increases in insulin sensitivity.

Bread Affects Clinical Parameters and Induces Gut Microbiome-Associated Personal Glycemic Responses: Cell Metabolism

numerous individuals exhibit opposite PPGRs to white and sourdough bread (Figure 4A). This result is further supported by previous evidence regarding the high interpersonal variability in PPGRs to real-life meals (Zeevi et al., 2015).

The Startling Link Between Sugar and Alzheimer's - The Atlantic

Melissa Schilling, a professor at New York University, performed her own review of studies connecting diabetes to Alzheimer’s in 2016. She sought to reconcile two confusing trends. People who have type 2 diabetes are about twice as likely to get Alzheimer’s, and people who have diabetes and are treated with insulin are also more likely to get Alzheimer’s, suggesting elevated insulin plays a role in Alzheimer’s. In fact, many studies have found that elevated insulin, or “hyperinsulinemia,” significantly increases your risk of Alzheimer’s. On the other hand, people with type 1 diabetes, who don’t make insulin at all, are also thought to have a higher risk of Alzheimer’s. How could these both be true? Schilling posits this happens because of the insulin-degrading enzyme, a product of insulin that breaks down both insulin and amyloid proteins in the brain—the same proteins that clump up and lead to Alzheimer’s disease. People who don’t have enough insulin, like those whose bodies’ ability to produce insulin has been tapped out by diabetes, aren’t going to make enough of this enzyme to break up those brain clumps. Meanwhile, in people who use insulin to treat their diabetes and end up with a surplus of insulin, most of this enzyme gets used up breaking that insulin down, leaving not enough enzyme to address those amyloid brain clumps.

Insulin under the influence of light -- ScienceDaily

To better assess the effect of light on tissue sensitivity to insulin, researchers measured insulin-induced glucose absorption. It turns out that a small disturbance in photic inputs (e.g. an hour of light exposure in the middle of the dark cycle, or light removal for 2 days) is enough to cause a negative effect. Indeed, increased or decreased light exposure can profoundly influence the sensitivity of tissues to insulin and the alteration, however minimal, of this mechanism is sufficient to significantly disrupt metabolic homeostasis. This would explain why people exposed to light at the wrong time -- workers in shift patterns, for example -- are more likely to develop metabolic diseases (e.g. diabetes).

Avocados, as a substitution for carbohydrates, can suppress hunger without adding calories: Meals that include fresh avocado can significantly suppress hunger and increase meal satisfaction -- ScienceDaily

The research found that meals including avocado not only resulted in a significant reduction in hunger and an increase in how satisfied participants felt, but also found that an intestinal hormone called PYY was an important messenger of the physiological response.

It's OK to indulge once in a while, study suggests: The body adapts to occasional short-term overeating: Body focuses on removing glucose to preserve insulin sensitivity in short-term overeating bout -- ScienceDaily

Although the amount of visceral fat that surrounds internal organs increased substantially, short-term overeating did not have a significant effect on the men's weight or fat mass. In addition, fasting levels of blood sugar and C-peptide -- an amino acid the body releases in response to increased production of insulin -- did not change. This finding was surprising because fasting levels of endogenous glucose -- new glucose the body produces in addition to what it has already stored for future use -- increased during the short-term trial. Chronic overeating increased the amount of total body fat and visceral fat as well as post-meal blood sugar and C-peptide levels. However, it did not alter fasting blood sugar levels, endogenous glucose production or the rate of glucose removal from the body (glucose disposal). This may be because the nutrient profile in the long-term trial was consistent with a typical diet and dietary fat percentages did not increase. Long-term overindulgence in fatty foods, instead of more nutritionally balanced foods, may be an important factor that causes rapid changes in blood sugar control.

How eating feeds into the body clock -- ScienceDaily

Dr Priya Crosby, a researcher at the MRC LMB and lead author on the study, highlighted: "Our data suggests that eating at the wrong times could have a major impact on our circadian rhythms. There is still work to do here, but paying particular attention to meal timing and light exposure is likely the best way to mitigate the adverse effects of shift-work. Even for those who work more traditional hours, being careful about when we eat is an important way to help maintain healthy body clocks, especially as we age."

Inactivity Induces Resistance to the Metabolic Benefits Following Acute Exercise. - PubMed - NCBI

METHODS: Ten untrained to recreationally active men (n=5) and women (n=5) completed a counterbalanced, crossover study. Four days of prolonged sitting without exercise (SIT) were compared to four days of prolonged sitting with a 1-hr bout of treadmill exercise (SIT+EX; 63.1±5.2% V̇O2max) on the evening of the fourth day. The following morning, participants completed a high fat/glucose tolerance test (HFGTT), during which plasma was collected over a 6-hr period and analyzed for triglycerides, glucose, and insulin. RESULTS: No differences between trials ( P > 0.05) were found in the overall plasma triglyceride, glucose, or insulin responses during the HFGTT. This lack of difference between trials comes with similarly low physical activity (~3,500-4,000 steps/day) on each day except for the 1-hr bout of exercise during SIT+EX the day before the HFGTT.

Seeing and smelling food prepares the mouse liver for digestion -- ScienceDaily

A previous study published in Cell in 2015 by another team of researchers found that sensory perception of food by lab mice was enough to trigger the neural pathways normally fueled by eating. Specifically, perceiving food inhibited AgRP neurons, which stimulate appetite, and activated POMC neurons, which induce satiety and suppress eating. The new study built on that research, focusing on how the changes in these neural pathways sent signals that affected metabolic activities in the liver. Here, the researchers found that within five minutes of lab mice perceiving food, the changes in POMC neuron activity were enough to induce a rapid signaling cascade that activated the mTOR and xbp1 signaling pathways. These pathways are normally activated when the liver takes up amino acids from digested food and help increase the protein folding capacity of the endoplasmic reticulum (ER), which assembles proteins from the amino acids found in food.

The case against carbohydrates gets stronger

We started the participants on a calorie-restricted diet until they lost 10%-14% of their body weight. After that, we randomly assigned them to eat exclusively one of three diets, containing either 20%, 40% or 60% carbohydrates. For the next five months, we made sure they didn’t gain or lose any more weight, adjusting how much food they received, but keeping the ratio of carbohydrates constant. By doing so, we could directly measure how their metabolism responded to these differing levels of carbohydrate consumption. Participants in the low (20%) carbohydrate group burned on average about 250 calories a day more than those in the high (60%) carbohydrate group, just as predicted by the carbohydrate-insulin model. Without intervention (that is, if we hadn’t adjusted the amount of food to prevent weight change), that difference would produce substantial weight loss — about 20 pounds after a few years. If a low-carbohydrate diet also curbs hunger and food intake (as other studies suggest it can), the effect could be even greater.

Insulin gives an extra boost to the immune system -- ScienceDaily

"We have identified one of metabolism's most popular hormones, specifically the insulin signaling pathway, as a novel 'co-stimulatory' driver of immune system function," says Dr. Dan Winer, who is also Assistant Professor, Department of Laboratory Medicine and Pathobiology at University of Toronto. "Our work characterizes the role of this signaling pathway in immune cells, mainly T cells, opening up avenues in the future to better regulate the immune system."