Affordable in home care | starts at $28 per hr

Monitoring Type 2 diabetes

Office of the National Coordinator for Health IT and Accenture Federal Services to demonstrate how patient-generated health data (PGHD) can best be delivered to clinicians and researchers to improve patient care and outcomes.

The federal pilot, which began in September 2016 and continues through August 2017, is a collaboration with Sutter Health, a 24-hospital health system in Northern California with over 11 million outpatient visits per year.

The pilot will focus on providing remote care and interventions using digital health devices to better manage and engage a population suffering from Type 2 Diabetes.

type-2

Genetics of Adipose Fat

The thrifty gene hypothesis (also called the famine hypothesis) states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally advanced in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains “as viable as when [it was] first advanced” in other contexts.[42][43]

In 1995, Jeffrey Friedman, in his residency at the Rockefeller University, together with Rudolph Leibel, Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked.[44][45][46] Leptin is produced in the white adipose tissue and signals to the hypothalamus. When leptin levels drop, the body interprets this as a loss of energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size.

Leptin, however, plays a different role in diet-induced obesity in rodents and humans. Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and – when leptin levels drop due to weight loss – hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety signal.[47] However, elevated leptin in obesity is known as leptin resistance. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research.[48]

Gene defects in the leptin gene (ob) are rare in human obesity.[49] As of July, 2010, only 14 individuals from five families have been identified worldwide who carry a mutated ob gene (one of which was the first ever identified cause of genetic obesity in humans)—two families of Pakistani origin living in the UK, one family living in Turkey, one in Egypt, and one in Austria[50][51][52][53][54]—and two other families have been found that carry a mutated ob receptor.[55][56] Others have been identified as genetically partially deficient in leptin, and, in these individuals, leptin levels on the low end of the normal range can predict obesity.[57]

Several mutations of genes involving the melanocortins (used in brain signaling associated with appetite) and their receptorshave also been identified as causing obesity in a larger portion of the population than leptin mutations.[58]

In 2007, researchers isolated the adipose gene, which those researchers hypothesize serves to keep animals lean during times of plenty. In that study, increased adipose gene activity was associated with slimmer animals.[59] Although its discoverers dubbed this gene the adipose gene, it is not a gene responsible for creating adipose tissue.

Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. Recent studies shed light into potential molecular mechanisms in the fate determination of pre-adipocytes although the exact lineage of adipocyte is still unclear.

Ectopic Fat

Ectopic fat is defined by the deposition of triglycerides within cells of non-adipose tissue that normally contain only small amounts of fat. Over the past decade, magnetic resonance spectroscopy has been used extensively for noninvasive quantification of intramyocellular, intrahepatocellular, and more recently myocardial and pancreatic lipids. In liver and muscle, triglyceride content usually correlates with whole-body and tissue-specific insulin sensitivity. However, fat mass and oxidative capacity influence this relationship, indicating that ectopic lipid content is not the only factor that explains insulin resistance. Ectopic lipids may rather serve as biomarkers of the balance between metabolic supply and demand in different states of insulin sensitivity. Consequently, ectopic lipid concentrations, particularly in the liver, decrease with lifestyle- or drug-induced improvement of insulin sensitivity.


Genes

Most cases of diabetes mellitus type 2 involved many genes contributing small amount to the overall condition.[1] As of 2011 more than 36 genes have been found that contribute to the risk of type 2 diabetes.[2] All of these genes together still only account for 10% of the total genetic component of the disease.[2]

There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes).[1] These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson-Mendenhall syndrome, among others.[1] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people.[3]

Polygenic

Genetic cause and mechanism of type 2 diabetes is largely unknown. However, single nucleotide polymorphism (SNP) is one of many mechanisms that leads to increased risk for type 2 diabetes. To locate genes and loci that are responsible for the risk of type 2 diabetes, genome wide association studies (GWAS) was utilized to compare the genomes of diabetic patient group and the non-diabetic control group.[4] The diabetic patients’ genome sequences differ from the controls’ genome in specific loci along and around numerous genes, and these differences in the nucleotide sequences alter phenotypic traits that exhibit increased susceptibility to the diabetes. GWAS has revealed 65 different loci (where single nucleotide sequences differ from the patient and control group’s genomes), and genes associated with type 2 diabetes, including TCF7L2, PPARG, FTO,KCNJ11,NOTCH2, WFS1, IGF2BP2, SLC30A8, JAZF1, HHEX, DGKB, CDKN2A, CDKN2B, KCNQ1, HNF1A, HNF1B MC4R,GIPR, HNF4A, MTNR1B, PARG6, ZBED3, SLC30A8, CDKAL1, GLIS3, GCKR, among others.[4][5][6][7]KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2(transcription factor 7–like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.[8] In addition, there is also a mutation to the Islet Amyloid Polypeptide gene that results in an earlier onset, more severe, form of diabetes.[9][10] However, this is not a comprehensive list of genes that affects the proneness to the diabetes.

Join 25,000 people in helping redefine health with health concierge and precision medicine.

https://clubalthea.com/2016/10/14/your-complete-dna-sequence-will-help-shape-the-future-of-medicine/

9 Super foods

Exit mobile version