Excess Fat
- Lafyva
- May 21, 2019
- 3 min read
Updated: Aug 6, 2024
Type 1 and type 2 diabetes have different causes. Yet two factors are important in both. You inherit a predisposition to the disease then something in your environment triggers it.
Hereditary haemochromatosis type 1 (HFE-related Hemochromatosis) [3] is a genetic disorder characterized by excessive intestinal absorption of dietary iron, resulting in a pathological increase in total body iron stores. [4] Humans, like most animals, have no means to excrete excess iron,[5] with the exception of menstruation which, for the average woman, results in a loss of 3.2 mg of iron.[6] Excess iron accumulates in tissues and organs, disrupting their normal function. The most susceptible organs include the liver, heart, pancreas, skin, joints, gonads, thyroid and pituitary gland; patients can present with cirrhosis, polyarthropathy, hypogonadism, heart failure, or diabetes. [7]
HOW DOES HAEMOCHROMATOSIS CAUSE DIABETES?
Haemochromatosis causes your body to absorb more iron than it needs from your food. This extra iron is stored in organs like the pancreas. It then damages the pancreas so the organ can't produce insulin properly. And we all need insulin to help glucose (sugar) get into our cells. People with untreated diabetes have too much glucose in their blood because they don't have enough insulin.
So a rise of iron in your blood can damage your pancreas. That means it can't produce insulin properly. And that is how secondary diabetes is caused by haemochromatosis.
Survive off body fat:
Obese Women:
" Thyroid hormone (TH) regulates metabolic processes essential for normal growth and development as well as regulating metabolism in the adult (28, 40, 189). It is well established that thyroid hormone status correlates with body weight and energy expenditure (80, 127, 143). Hyperthyroidism, excess thyroid hormone, promotes a hypermetabolic state characterized by increased resting energy expenditure, weight loss, reduced cholesterol levels, increased lipolysis, and gluconeogenesis (26, 184). Conversely, hypothyroidism, reduced thyroid hormone levels, is associated with hypometabolism characterized by reduced resting energy expenditure, weight gain, increased cholesterol levels, reduced lipolysis, and reduced gluconeogenesis (27). "
Atlas of exercise metabolism reveals time-dependent signatures of metabolic homeostasis
Highlights
•Time of exercise defines system-wide activation of energy metabolism
•Exercise timing rewires intra-tissue and inter-tissue metabolite correlations
•Maintenance of inter-tissue metabostasis is specified by exercise time
•Comparative analyses reveal time- and tissue-dependent exerkines
Germ-Free Mice Gnotobiotics https://ods.od.nih.gov/factsheets/VitaminK-Consumer/ "Life in a Germ-Free World": Isolating Life from the Laboratory Animal to the Bubble Boy
The MK-4 form of vitamin K2 is produced by conversion of vitamin K1 in the testes, pancreas, and arterial walls.[32] While major questions still surround the biochemical pathway for this transformation, the conversion is not dependent on gut bacteria, as it occurs in germ-free rats[33][34] and in parenterally administered K1 in rats.[35][36] In fact, tissues that accumulate high amounts of MK-4 have a remarkable capacity to convert up to 90% of the available K1 into MK-4.[33][34] There is evidence that the conversion proceeds by removal of the phytyl tail of K1 to produce menadione as an intermediate, which is then condensed with an activated geranylgeranyl moiety (see also prenylation) to produce vitamin K2 in the MK-4 (menatetrenone) form.
Personality traits of aggression-submissiveness and perfectionism associate with ABO blood groups through catecholamine activities
Personality trait research has shown associations with many genes, prominently those of the catecholamine metabolism such as dopamine beta hydroxylase (DBH), catechol-O-methyltransferase (COMT), and monoamine oxidase A (MAOA). Because DBH gene is in linkage disequilibrium with ABO gene, there is reason to think that other catecholamine genes using the same substrate as DBH may also have associations with ABO blood groups, and this paper demonstrates how this may be so.
