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Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease | Endocrine Reviews | Oxford Academic
metabolic flexibility can be placed in the broad context of health and disease and a deeper understanding of its intricacies will significantly affect health care. As a final note, the situation portrayed here does not necessarily reflect that of each individual. Because of the genetic and epigenetic disparity of humans and the enormous varieties in lifestyle, it is not unthinkable that each person fashions a unique way to maintain energy homeostasis. In light of the rapid developments in the field of nutrigenomics and personalized medicine, future research will likely focus on the union between metabolic flexibility and personalized medicine.
metabolic  metabolism  flexibility  evolution  genetics  epigenetics  individual  variation  endocrine  neurotransmitter  hormone  insulin  peer-reviewed  research  pathophysiology  risk  genetic  factor  energy  homeostasis 
august 2018 by Michael.Massing
Diet-induced insulin resistance precedes other aspects of the metabolic syndrome. - PubMed - NCBI
This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.
insulin  resistance  metabolic  syndrome  factor  risk  etiology  diabetes  in  vivo  animal  peer-reviewed  research  diet  high  fat  sugar  complex  carbohydrate  low  symptoms 
january 2018 by Michael.Massing
Diet-induced insulin resistance precedes other aspects of the metabolic syndrome | Journal of Applied Physiology
This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.
insulin  resistance  metabolic  syndrome  factor  risk  etiology  diabetes  in  vivo  animal  peer-reviewed  research  diet  high  fat  sugar  complex  carbohydrate  low  symptoms 
january 2018 by Michael.Massing
Amish Mutation Protects Against Diabetes and May Extend Life - The New York Times
What Dr. Vaughan and his colleagues discovered was striking. Amish carriers of the mutation live on average to age 85, about 10 years longer than their peers. Among the Amish who did not have the mutation, the rate of Type 2 diabetes was 7 percent. But for carriers of the mutation, the rate was zero, despite leading the same lifestyle and consuming similar diets. Tests showed that carriers of the mutation had 28 percent lower levels of insulin, a hormone whose chronic elevation can lead to Type 2 diabetes.
news  org:rec  genetics  genomics  pop-diff  recent-selection  usa  midwest  longevity  health  hetero-advantage  cardio  metabolic 
november 2017 by nhaliday

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