Thrifty gene hypothesis obesity - …
01/05/2006 · Thrifty genes for obesity and the metabolic syndrome — time to call ..
the thrifty gene hypothesis, ..
Studies of different human populations indicate that human evolution continued not only after we branched off from apes, but even long after Paleolithic times. Some studies suggest that people whose ancestors came from warm, lowland environments, who had to work hard for all their meals even after food became abundant elsewhere, tend to have slow metabolisms, and people whose ancestors came from cold, highland environments tend to have high metabolisms. While one group had to survive long periods of famine, the other group likely had to metabolize lots of animal fat. What both groups have in common are lifestyle diseases in response to a modern Western diet and sedentary mode of living. There is some debate about whether gene variants leading to type 2 diabetes really resulted from periods of food scarcity ("thrifty gene hypothesis") or whether they just resulted from genetic drift ("drifty gene hypothesis").
The most exciting recent hypothesis adjusts the notion of “thrifty genes”, genetic variants that promote the acquisition and storage of calories, to that of “drifty genes”, genetic variants that have not been selected for or against during most of human evolution and which are somewhat randomly distributed throughout human populations, but which now, in the face of abundant food availability, strongly influence why some people are predisposed to becoming fat while others effortlessly remain lean.
"This thrifty gene theory is an ..
More striking than similarities among great apes are DNA similarities between a much wider range of animals. Analysis of human versus fruit fly DNA indicates that we use basically the same genes, just in different ways with different combinations and different timing. Scientists have also pinpointed some specific genes that do different things in different organisms. Research led by Arhat Abzhanov of Harvard University suggests that a gene that geneticists have dubbed BMP4 both strengthens the jaws of fish that eat a robust shellfish diet, and bulks up beaks of Galápagos ground finches. A 2015 study by Sangeet Lamichhaney and coauthors found that a different gene, ALX1, plays a strong role in beak formation in Darwin's finches, as well as facial structure in humans. Another gene identified as FOXP2 helps young finches learn to sing, and young humans to speak.
And then there are genes that manage the big picture in a variety of organisms. First found in fruit flies, Hox genes regulate overall body plans for everything from bugs to birds. Although the genes differ between vertebrates and arthropods, they show remarkable similarities. They often occur together in a comprehensible order, in contrast with most other genes, and their order matters. Arguably grisly experiments with these genes show that moving them around creates fairly disgusting mutants, like flies with legs sprouting from their heads. Likewise, grafting mouse mouth tissue into a developing chick embryo demonstrates how Hox genes work across different animals; the resulting chicks hatch with teeth, though the teeth look dinosaurian.
Thrifty Gene Hypothesis - download photos, textures
Biologists and paleontologists have made a convincing case that life diversified tremendously during the Cambrian, and that the body plans apparent half a billion years ago showed significant similarities to body plans still thriving today. Figuring out why, and why then, is more challenging. Possible triggers include environmental changes, such as the retreat of the glaciers of Snowball (or Slushball) Earth, or the increased availability of oxygen, though those big changes happened before the Ediacaran Period. The development of predation might have spurred an evolutionary arms race, though that becomes a chicken-and-egg question of timing. Another possibility involves changes in developmental genes. Although evolution is not random, it can be driven by random changes in genes, and changes in Hox genes responsible for regulating overall body plans could have contributed to a rapid diversification of animal phyla over a short span of geologic time. Genetic changes might also have limited the diversification of phyla after that time. Evolution certainly continues today, but it doesn't appear to operate at the phylum level in the animal kingdom.
The Eocene Epoch began roughly 10 million years after the last dinosaurs went extinct, so the epoch lasted from about 55 million to 34 million years ago. The Eocene and brought primate-friendly greenhouse conditions, where rainforests covered huge expanses of our planet. Primates thrived not just in Africa and Asia, but also Europe and North America. Primates lived in Wyoming! The ensuing epoch, the Oligocene (34 million to 23.5 million years ago) experienced cooler, drier conditions. On a planet less welcoming to primates, many species went extinct, though plenty survived in Africa and Asia. And even though the planet was cooler and drier than it had been in the Eocene, it was still generally warmer than it is now. Even in the Miocene Epoch (23.5 million to 5.3 million years ago), rainforests remained abundant, and the number of primate species living then likely dwarfed the number of primate species living today.
Time of Onset of Non-Insulin-Dependent Diabetes …
Genetic causes of diabetes mellitus type 2 - Wikipedia
The thrifty gene theory ..
Pathogenesis of type 2 diabetes mellitus - …
What if It's All Been a Big Fat Lie
Time of Onset of Non-Insulin-Dependent Diabetes Mellitus and Genetic Variation in the β 3-Adrenergic–Receptor Gene
Razib Khan's GNXP - Gene Expression
Speakman has come up with an alternative theory, nicknamed the ‘drifty gene’ hypothesis. He argues that the modern distribution of obesity stems from a genetic drift in the genes encoding the system that regulates metabolism and controlling an upper limit on our body fatness. Such a drift may have started because around 2 million years ago when ancestral humans ceased to be prey, which was probably a key factor maintaining the upper boundary of the regulation system.
Genetics & the Jews - Gene Expression
In the 1960s, the American geneticist James Neel developed what became known as the “thrifty gene” theory to explain the increase in obesity that lay behind a rise in diabetes. According to his hypothesis, the thrifty genotype would have been advantageous for early humans allowing them to store fat in times of abundance and survive in times of food scarcity. In modern societies with an abundance of food, this genotype prepares individuals for a famine that never comes. The result is obesity and diabetes.
20/03/2003 · Original Article
Bacteria generally reproduce so quickly that humans can observe multiple generations in the space of a day, and this has enabled scientists to observe evolution. Experiments published in 2013 tested multiple generations of a bacteria species that occurs everywhere from soil to human skin to human lungs, . Placing the microbes in petri dishes with tasty bacteria food, the researchers let the microbes evolve, took samples after 24 hours, and let the sampled microbes start their own colonies. Within days, the strains had evolved into "hyperswarmers" that were incredibly fast at fanning out to find new food. The bacteria evolved extra tails (microbes in the original strain were single-tailed), thanks to mutations in a gene known as FleN. But not all the new bacterial strains were the same; the scientists identified three different types of tail configuration. The evolution in these bacteria was swift and unmistakable, but apparently came at a cost. Another ability needs to thrive is the ability to build a film over the colony — something that has made fighting infections from this bug very difficult. And when it comes to film building, single-tailed bacteria out-compete the multi-tailed fast movers.
Sadaf Farooqi, M.D., Ph.D., Julia M
Human brains can pose problems at both the beginning and the ending of life. We are more intelligent than our ape relatives, but at a price. A study published in 2015 suggests that the same genes responsible for increased neuron connectivity may also lead to Alzheimer's — a condition not known to afflict any other animal, not even great apes.
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