Metabolic Diseases - Science topic

There are well-established links between diet and the development of chronic metabolic diseases such as insulin resistance, type 2 diabetes, obesity, and cardiovascular disease. Diets high in refined carbohydrates, sugars, saturated fats, and processed foods are associated with an increased risk of metabolic disorders, while diets rich in whole grains, vegetables, fruits, and lean proteins are protective.

Links Between Diet and Chronic Metabolic Diseases:

Link Between Insulin Resistance and Ghrelin Resistance:

Ghrelin, known as the "hunger hormone," stimulates appetite and is involved in energy homeostasis. Recent research suggests a link between insulin resistance and ghrelin resistance, especially in the context of obesity:

References:

We can be happy when we are healthy if we are not healthy then we cannot enjoy life. We always think about our body problems. Nowadays days Diabetes and other metabolic problems are epidemic in the world. And no medicine or substitute to cure them. The main causes of metabolic disorders are remineralisations of saliva, lipids hormones and biosynthesis in our body. To solve the problems Please read the book “Your Health Is In Your Mouth” Links: - https://www.amazon.in/Health-Mouth-Innovator-Pramod-Stephen/dp/1387414453English

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Hello Amjad Mahmood Qadir

If you notice at the cellular level, homeostasis is observable in the biochemical reactions that take place. Regulation of pH, temperature, oxygen, ion concentrations, and blood glucose concentration is necessary for enzymes to function optimally in the environment of the cell, and the formation of waste products must be kept in control as not to disrupt the internal environment of the cells as well. The cell will remain alive as long as the internal environment is favorable and can be a functioning part of the tissue to which it belongs.

So, maintaining homeostasis (self-regulating process by which stability is maintained while adjusting to conditions that are best for survival) is important as it ensures that the body's internal milieu remains steady and continuous, enabling it to function at its best, and is crucial to its daily activities.

2. Relationship between genetic mutations and metabolic disorders.

Metabolism is a complex set of chemical reactions that your body uses to maintain life. These include making energy such as special enzymes that break down food or certain chemicals so your body can use them right away for fuel or store them for later use, and getting rid of substances that your body no longer needs. When these processes don't work properly, a metabolic disorder occurs. It may be due to an enzyme that's too low or missing or due to another problem.

Most metabolic disorders are caused by the genetic deficiency of an enzyme that is needed to convert one chemical into another. Whenever a random mutation happens in the coding DNA that codes for the enzyme, wrong amino acids could be used to make the enzyme. This could change the shape of the enzyme's active site resulting in an enzyme that does not function normally.

You may have heard about Inherited Metabolic Disorders which are medical conditions caused by changes in specific genes that affect metabolism. Different gene changes cause different types of Inherited Metabolic Disorders. These gene changes are mostly passed down from both parents. But sometimes the gene change comes only from one parent, most often from the mother. These disorders are also called Inborn Errors of Metabolism.

For instance, Gaucher's disease which you have mentioned, is an inborn error of metabolism due to the accumulation of glucocerebroside lipids. Toxic accumulation inborn errors of metabolism fall into 3 major categories: localized toxicity, circulating toxicity, or a combination of both. Gaucher's disease is an example of localized toxicity.

Another example is Phenylketonuria (PKU) which is an inherited disorder that increases the levels of a substance called phenylalanine in the blood. PKU is caused by mutations in the gene that helps make an enzyme called phenylalanine hydroxylase (PAH). This enzyme is needed to convert the amino acid phenylalanine into other substances like tyrosine which the body needs. When this gene, known as the PAH gene, is defective, the body cannot break down phenylalanine. As a result, phenylalanine accumulates and is toxic to the brain. Without treatment, most people with PKU would develop severe intellectual disability.

Hope this explanation is helpful!

Best.

Good answer, But, Can you say that or give proof like diabetes or any other metabolic abnormities cured by medications, dietary changes, and lifestyle modifications?

Yes, gout is considered a metabolic disease. It is a type of arthritis that results from the buildup of uric acid in the body, typically due to the body's inability to process or excrete it properly. This condition is often associated with metabolic factors such as diet, obesity, and genetics.

The metabolic cause of gout is primarily due to deficiency or alteration in the enzyme called xanthine oxidase. Xanthine oxidase is responsible for catalyzing the conversion of hypoxanthine and xanthine to uric acid as part of the purine degradation pathway. This enzyme plays a critical role in the final step of purine metabolism, leading to the production of uric acid. An excess of uric acid in the body, often due to factors such as diet, genetics, or kidney function, can contribute to conditions like gout, where uric acid crystals can accumulate in joints, leading to pain and inflammation. Drugs like allopurinol like allopurinol can be used to treat gout. Allopurinol is a medication commonly used in the treatment of conditions like gout and hyperuricemia (high levels of uric acid in the blood). It works by inhibiting the enzyme xanthine oxidase, which is involved in the production of uric acid. By reducing the activity of xanthine oxidase, allopurinol helps lower uric acid levels in the body. This, in turn, can prevent gout attacks and reduce the risk of uric acid crystal formation in joints and other tissues. Allopurinol is typically taken orally as a prescription medication and is considered a long-term treatment for managing conditions related to excessive uric acid production.

The first type of diabetes that occurs in our body is Diabetes type 1 and after a long time of treatment our body becomes resistant to the medicine and it converts into diabetes type 2 it gens goes to our fetus and develops from generation to generation. For Metabolic disorders read my book:-"Your Health Is In Your Mouth"

In India, several genetic diseases are frequently observed, reflecting the country's diverse population and genetic landscape. Among the most prevalent are thalassemia and sickle cell anemia, particularly in regions like Punjab, Gujarat, and eastern India. Cystic fibrosis is also found, albeit less commonly, affecting the lungs and digestive system. Congenital heart diseases, including atrial septal defect and ventricular septal defect, have a higher prevalence, necessitating specialized medical care. Additionally, G6PD deficiency is notable, especially in malaria-endemic areas. These genetic disorders underscore the importance of genetic counseling, early diagnosis, and management to improve the quality of life for affected individuals and reduce their transmission to future generations.

"Wherever your body hurts your soul is there" used to say our older generations. Which seems to be quite correct since animals have interconnecting blood vessels and neurons covering almost all body.

Hello!

Ascites in broiler chickens results from an imbalance between the amount of oxygen available and the amount needed to maintain rapid growth rates and high feeding efficiency. Ascites is influenced and/or caused by variables such growth rate, altitude (hypoxia), and ambient temperature because of the link to oxygen requirement.

Toxins from plants like Crotalaria or aflatoxin may harm the liver in chicken. Obstructive cholangiohepatitis, which is brought on by an infection with Clostridium perfringens, is the most typical cause of liver damage and ascites in broiler chickens. Ascites can result from hepatic amyloidosis in breeders as well as meat-type ducks.

For a more detailed explanation, please refer to this article:

Hargis, B. M. (2022, August 4). Ascites syndrome in poultry - poultry. MSD Veterinary Manual. from https://www.msdvetmanual.com/poultry/miscellaneous-conditions-of-poultry/ascites-syndrome-in-poultry

Please go through the following RG links.

nice survey , good job

i think most of the surgeon well try sleeve gastrostomy as first choice , because of the easy of the surgery and the comparable result to bypass.

Maybe of interest:

Regards,

Joachim

I fallowing

One example in the positive: Fingernail splintering is not uncommon and is effectively treated by adding gelatin powder to your morning orange juice. I think this may be more important than one realizes since gelatin is the precursor of collagen and collagen is 30% of all the formed protein in the body. Splintering finger nails may be the tip of the iceberg.

Perhaps the “ESPGHAN/ESPEN/ESPR guidelines on pediatric parenteral nutrition: Carbohydrates” and related publications provide the appropriate and practical instructions for glucose infusion in children [1]. Excessive chronic glucose infusion may lead to hyperglycemia, which leads to increased lipogenesis and adipocyte fat deposition along with subsequent hepatic steatosis, elevated hepatic VLDL triglycerides, hypercholesterolemia, and may ultimately cause insulin resistance (IR) [1]. The magnitude of this effect depends individually and is affected by pre-existing metabolic stress or disease [1]. The gold standard for determining IR is the euglycemic–hyperinsulinemic clamp technique [3]. This method is considered invasive, costly, and impractical for large samples. Despite its modest specificity and sensitivity, HOMA-IR is used as an IR surrogate and alternative index in a large number of studies, including those dealing with children [4]. Other IR indexes with varied specificity and sensitivity, as well as purposes, are available [3,4].

References:

[1] Mesotten D, Joosten K, Kempen A, et al. ESPGHAN/ESPEN/ESPR guidelines on pediatric parenteral nutrition: carbohydrates. Clinical Nutrition, 2018; xxx: 1-7. http://dx.doi.org/10.1016/ j.clnu.2018.06.947.

[2] Sanchez-Garc´ıa A, Rodr´ıguez-Gutierrez R, Mancillas-Adame L. et al. Diagnostic accuracy of the triglyceride and glucose index for insulin resistance: a systematic review. International Journal of Endocrinology, 2020; ID 4678526, 7 pages. https://doi.org/10.1155/2020/ 4678526.

[3] van der Aa Marloes P, Catherijne AJK, Anthonius dB, et al. Definition of insulin resistance affects prevalence rate in pediatric patients: a systematic review and call for consensus. Journal of Pediatric Endocrinology and Metabolism, 2017; 30(2):123-131.doi:10.1515/jpem-2016-0242.

Feng J, Xing W, Xie L. Regulatory Roles of MicroRNAs in Diabetes. Int J Mol Sci. 2016 Oct 17;17(10). pii: E1729. Review. PubMed PMID: 27763497; PubMed Central PMCID: PMC5085760.

Yes, we need approaches to study their activity in vivo.

Please see the following PDF attachments.

Great question.

I was researching similar myself. GLUT4 would, apparently be less active at the surface. GLUT4 status and ChREBP influence each other via a few feedback loops.

Hi Romina, if that's the case, you can simply centrifuge the bacteria culture and apply the ferulic acid-rich supernatant to your cell culture. I guess you have certain kits to measure the ferulic acid level? As long as your concentration is the same as your commercial preparation, you should be fine. I do not recommend loading bacteria into the culture, alive or dead, because bacteria components may cause the cells to alter expression profile, hence you cannot be sure whether the change you observe is due to bacteria or the ferulic acid.

Fish and fish products, including salmon, herring, sardines, cod liver oil and tuna, are rich from vitamin D. Moreover, egg yolk and mushroom are also good soruces of vitamin D

A very interesting exchange. I refer you all to a new review i had written on how hyper-insulinemia can cause insulin resistance (Najjar and Perdomo, Physiology, May issue-2019).

Hi Go,

Physiologically, GRP78 is a protein chaperone that maintains proper protein folding. Under normal conditions, GRP78 is normally found bound to ER membrane proteins, PERK, IRE1, and ATF6, keeping these proteins in an inactive state. When cellular events occurs, as Muruganandan Shanmugam addressed, GRP78 dissociates and allows each of PERK and IRE1 subunits to undergo homodimerization and ATF6 cleavage. This process activates the unfolded protein response.

However, there is a strange paradigm shift that is currently occurring in today's literature. In conditions of cancer, GRP78 is somehow able to escape the ER and relocate itself to the cell surface. It can associate itself with other cell surface receptors. Furthermore, auto-antibodies against GRP78 is able to trigger intracellular signalling.

Inherited metabolic disorders are genetic conditions that result in metabolism problems. If it's can considered as linking so most people with inherited metabolic disorders have a defective gene that results in an enzyme deficiency. There are hundreds of different genetic metabolic disorders, and their symptoms, treatments, and prognoses vary widely.

Follow

Fruits without processing them an in moderate Portion sizes are beneficial. For fiber to give feelings of fullness and essential vitamins, berries, oranges, apricots, and apples are goood. For diabetIcs, they can be good with A1C and fighting inflammation.

Neuropathy is equivalent to computer CPU hardware malfunction, psychosis is equivalent to software malfunction. In my opinion, people's mental and psychological activities are a set of programs, which are similar to computer programs. Psychosis is a disorder of procedure. Enclosed are my papers on this subject

Hi Yanuar

I've found lots of old papers in rats. Handling rats is always easier, their brain and bodies are x10 times larger, everything is easier with them. But since genetically modified animals are usually mice, they have become the species-of-use in the last two decades.

Optogenetics and pharmacogenetics can be done in rats as well, provided you get viral vectors designed for rats, which is not so difficult.

Both species are similar but not identical. Both are rodents, and good models for studying interesting issues for humans, I don't find advantages in mice or rats relative to their similarity to humans.

Good luck

Fernando

Vitamin D has well established effects on mineral metabolism, skeletal health, and recently established effects on the cardiovascular and immune systems. Vitamin D deficiency is highly prevalent and evidence is mounting that it contributes to the morbidity and mortality of multiple chronic diseases, including systemic lupus erythematosus.

Please have a look at these useful RG links and PDF attachments.

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I spent some time in eastern Africa as an environmental officer, my home was in Nairobi. On an assignment to Uganda, I ran across an old Brit MD and we discussed heart and vascular disease. He commented that the local diet was high in fat but that the prevalence of heart disease was low but had increased following the establishment of sugar plantations and refineries.

The fat may impact the ability of the endothelial cell to generate NO and the sugar generate ROS, thus pro inflammatory transcription factors, hence upregulation of ICAM-1

See, for example: Mitochondrial Reactive Oxygen Species Mediate Lysophosphadylcholine-induced Endothelial Cell Activation, by Xinyuan Li, et al.

Dr Edo McGowan

Dear Dr Malik,

maybe the following link can help you. It is a relatively recent paper, which is even linked on researchgate:

Yours sincerely,

Rainer

There are many factors that may affect weight loss as physical activity. We can expect healthy loss of weight based on a dietitian diet for 20 to 25 kg

Dear colleague,

As I see it, the classic has its charms. Drug-induced diabetes, such as in streptozotocin models, are not only prevalent in the literature, but also current. I found these interesting reviews on the topic:

And, of course, you can aways see what the companies are producing:

Sincerely,

Hércules Freitas

May be, Immune system cells recognize their own tissue and show self-tolerance.

There are also healthy normal cells that control the immune system cells. However, genetic hormonal or environmental factors can change this balance. Because of this, the induction of autoimmune diseases is not dependent on endocrine and metabolism.

You ask an important question with far ranging implications and complex solutions.

I think the best framework to use in approaching this question is a model developed for  the US Institute Medicine. In practical terms, it recommends four categories of care (Wellness Basics, Restorative Therapies, Symptom Relief, Over-care avoidance - these are not the names they use, but are ones that are much easier to grasp).

I think the best way to answer your question is to  restate it, "what is the best way to optimize physical health in each of the four categories of care, for someone with severe mental illness?". I think the restatement is important, because the answers in each category are different. Typically, activity is required in all categories at the same time. In addition, these approaches are best deployed within the context of a recovery model of evolutionary improvement and ever-increasing self-determination.

I'll assert the highest level answer in all four categories.

Wellness Basics. These include 1) Housing & Security, 2) Diet & Digestion, 3) Exercise & Sleep, 4) Calm Awareness, 5) Effective Self-Management, 6) Purpose & Meaning, 7) Social & Outer Engagement, 8) Belief, Hope & Self-Transcendence. There are hundreds of RCTs that support that doing the right things in these areas directly support both mental and physical health. For instance, housing is the absolute first thing that one must do to support the physical wellness of someone with severe mental illness. Without it, their life nearly always remains in shambles. Approaches to wellness in this category are normal disciplines of wellness for everyone and are fairly well understood, though not always within reach. The challenge here is that these approaches often requires self-determination and lifestyle changes, things that can be extremely hard for people with severe mental illness. But, the good news here is that most of these things do not require medical intervention and can often, with a little creativity, be found without huge expense.

Restorative Therapies. These are mental health interventions targeted at suspected root causes of mental health symptoms, divided into two groups: Biomedical and Psychosocial. The Biomedical ones are directly tied to both physical health and mental health. Things like Nutrient therapy, Pathogen therapy, Endocrine therapy, Food Allergy Therapy, detoxification therapy, etc. are all therapeutic responses to physical issues that are well-known to potentially cause mental health symptoms. Approaches to wellness in this category are squarely within the medical discipline. It demands - though it is rare in conventional psychiatry today - robust biomedical testing. This testing is one of the cornerstones of integrative psychiatry, which is producing recovery rates substantially higher than those from drug therapy alone (the best evidence of this is through extensive open-label trials with Nutrient Therapy). Dr. Michael First, editor of the DSM-5 laments that current psychiatry often jumps to symptom-based diagnoses and all but avoids step three of the differential diagnosis process (the step that looks for underlying causative issues).

Symptom Relief. Effort here is to relieve residual mental health symptoms that the first two categories don't address. Psychotropics are by far the most common option here, but there are others with a smaller, but non-trivial evidence base: herbs, very small current electro-stimulation devices (like tDCS, tACS, CES, etc.), sensory therapy, etc. This area is predominantly tangential to the issue of physical health, with one exception. Symptom relief to some degree is often a mandatory first step to achieve stabilization. It is only after some measure of stabilization that we can even begin to consider improving physical health through approaches in the first two categories of care.

Over-care avoidance. This is a huge challenge in psychiatry today. Ill-advised polypharmacy and off-label prescribing, prescribing at dosages over recommended levels, over prescribing of psychotropics to vulnerable populations (the elderly, veterans, foster children...) and probably the most detrimental - antipsychotic polypharmacy - have been known to substantially impact physical health negatively. These are well understood by the APA and they have campaigns to reel-in some of these, especially antipsychotic polypharmacy. This has a huge implication on physical health. Outcomes from overcare are stark: significantly increased chances of death and a far ranging list of serious side effects.

So, how do we ensure the physical health of people with severe mental illness? 1) Focus outside of the medical discipline on the most out-of-balance wellness basics to establish new healthier lifestyle choices, 2) through robust biomedical testing, search for and address any physical issues found that are commonly known to cause mental health issues, 3) do enough symptom relief to reach a measure of stability so that a focus on physical health can be begun, 4) be ever vigilant to avoid over-care and seek "minimal effective dosages", starting dosages small and ramping slowly, 5) deliver these wellness approaches within the context of a recovery model that maximizes self-determination and recognizes that recovery is an iterative, evolutionary process where setbacks are common.

To deliver the above in a coordinated way is extremely difficult today and, to be done well, requires a holistic approach to patient care. I think to make substantive progress, we need to adopt something similar to this 4-categories of care model and train case workers on its fundamentals and how they can help individuals map into available services in each area.

Interesting question, probably in cells of patients GSH is not depleted, due to the fact that they can use cysteine whose origin is not methionine/hCys (Trans sulfurathion patwhway). Do you have any reference for GSH levels in tissues these patients? I have performed some experiments with cells with methionine free medium whose cysteine levels (and GSH too)  is minimally influenced by the absence of methionine.

I would be very interested to know if anyone has any idea of how many FARA's are still used routinely. No scientific basis for my request, just that I was a Roche customer for many years from 1978, first with Centrifichem, COBAS BIO and then FARA...then I worked for Roche for the past 26 years and will retire next year. For me the FARA was the most wonderful and flexible invention, and I was able to automate so many applications in my lab at that time. It would be nice to give it a mention in my closing speech...there are are still people working here in R&D in Switzerland who remember it fondly...

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Swimming or aquatic exercise may not be the best form of exercise for McArdle patients simply because it may challenge their balance and if they have to rapidly correct, it will cause a rapid muscle contraction which could lead to a contracture.

The advice for most patients with this condition would simply be to use walking in their everyday lives. Overload is useful for applying a stimulus; that will cause adaptation and, ultimately improve function. However, it is very important that all individuals with McArdle disease start exercise at a very low intensity. Even this can elicit pain and so the patient may need to slow down or stop until the pain has reduced or has gone. They should then start walking again or walk a little faster, this process should, continue until they reach a pace that they can walk at for around 10 minutes. Over 12-16weeks, it should be possible to increase the duration of walking until they are able to walk continuously with no, or only very mild, pain for 30 minutes. The ultimate plan is to build this up until patients are able to take 150 minutes of exercise per week. This is the recommended amount of exercise suggested by most guidelines as the minimum required to reduce risks to health. Of course, being a minimum, people should aim to do even more.....but one step at a time!

You can use Autodock 4.2, Autodock Vina, Python etc software to determine the bacterial interaction with proteins. Below references will be helpful for you.

1. http://www.ncbi.nlm.nih.gov/pubmed/?term=Kinetic+and+molecular+docking+studies+of+loganin+and+7-O-galloyl-d-sedoheptulose+from+Corni+Fructus+as+therapeutic+agents+for+diabetic+complications+through+inhibition+of+aldose+reductase

2. http://www.sciencedirect.com/science/article/pii/S2211383514001014

Whereas severe hypophosphatemia may lead to acute hemolytic anemia, decreased myocardial contractility, neuromuscular disturbance, respiratory weakness or even rhabdomyolysis and altered mental status, its impact on survival remains questionable.

At evidence no effect in DKA In contrast with a potential prognosis factor in case of AKI which received CVVH therapy.

Even, if we observed rare case of acute severe hypophosphatemia in acute exacerbation of COPD, its role on respiratory failure could not be established: severe respiratory acidosis or metabolic alkalosis during the first days of mechanical ventilation???

Two publications could be helpful, but the question remains of interest.

Rangarajan, what fails as therapy for one population may work for another. As for lifestyle intervention, this is a radical change in eating behavior and attitudes towards eating and physical activity that starts with small changes. The thinking about health has to change first and the behaviors need to follow. For example, a lifestyle change for persons with type 2 diabetes could be exchanging fried food with baked food or using the stairs instead of the elevator. Patient selection refers to making a scientific study by narrowing the differences between the patients in areas of length of time with diabetes, previous diabetes education, culture/ethnic health beliefs...etc.

Oligodendrocyte-specific protein (OSP/claudin-11) is a four transmembrane protein concentrated in central nervous system myelin. Recent evidence has emerged suggesting that OSP/claudin-11 is involved in membrane interactions at tight junctions and with the extracellular matrix. OSP/claudin-11 seems to modulate proliferation and migration of oligodendrocytes presumably through these interactions. Furthermore, evidence is presented implicating OSP/claudin-11 as an autoantigen in the development of autoimmune demyelinating disease.

J Neurosci Res. 2000 Mar 15;59(6):706-11.

I have read the given answers, but should like to add the following: You should differentiate between the sphingosine accumulaton in NP disease type C (NPC; defective NPC1-protein) and that in NP types A and B (acid sphingomyelinase/SMPD1 defect). In NPC lipds aside of cholesterol are accumulated within the lysosome but sphingomyelinase, though low, is still present, as is acid ceramidase. Due to the lipid trafficking jam, enzymatically released sphingosine cannot be released from the lysosome nor be re-utilized, therefore it may accumulate, and eventually, after cell death, even (partially) appear in blood plasma. To this process (if true), there may add a similar process, but starting from glycolipids (for, example, lac-cer and Gb3 which are also accumulated), leading to additional sphingosine enhancement.

In NPA/B (sphingomyelinase deficiency), sphingomyelin-derived ceramide and subsequent sphingosine release should be low, but there may be also some secondary lipid trafficking jam out of the lysosome, suggested by some cholesterol accumulation also seen in NPA/B, which, secondary to the lysosomal sphingomyelin accumulation, may lead also to some lysosomal retention of glycolipid-derived sphingosine, which may become enhanced as described above.

I am not very sure about my hypothesis, but I think it could be discussed.

In the context of Haemochromatosis :

In critical geriatrics inpatients you should always think if there is a subclinical Addison's disease in order to supplement a little of corticosteroid and get better results in your therapy and toward  the recover of the patient

In the following paper a calibration methodology for metabolic analyzer and the estimation of uncetainty have been described.

I am not unbiased, as you can imagine. The answer also depends on your objectives. I am skeptical about the distinction about aging and age-related diseases and also try to avoid going to semantics. There are many biomarkers of aging but all they are "weak", in a sense. Using the frailty index approach we can find a summary measure that is much superior to any single biomarker.  Aging is a systemic property of the organism therefore any assessment should also be systemic, i.e. to combine available information.  Such information can be based on clinical assessment  or even self-reports but also can be more "objective". Take a look at the recent paper Howlett et al. BMC Medicine, 2014 where the lab tests were combined together in a FI-Lab. To go in this direction you should not hate math, although math is very basic.

Arnold

Successful management requires identification and addressing both root cause, barrier. Patient vary considerably in their readiness and capacity. Success can be defied as better quality of life. greater self esteem. higher energy level etc. There is an approach for obesity management from Canadian obesity network: www.obesitynetwork.ca

although most of research on obesity is concenrating on white adipose tissue and the development,differentiation ie hypertrophy and hyperplasia of adipocytes and pfeadipocyytes in WAT and role of inflammation and macrophage infiltration directly or conversion of preadi[ocytes,metabolic endotoxemia,gut microbiota lreading to increased LPS absorption from increased GIT permeability with altered gut microbiota is some of the aetiopathogenesis with infiltration of Treg cells,cdt4. CHT8 cellsiNKT CELLS th17 all have ben found but importance is being given simultaneously to the microrna which affect the differentiATION OF BRITE AND BROWN ADIPOCYTES AND IMPORTANCE OF MIrna'S 26,155,27a,b,130 a ,miR155 etc in adipocyte differentiation and how further roles of FGF21 may affect thermogenesis and natriureteic peptides

I would recommend the most "normal" formulation you can find. In my lab, we use Humulin R, but any simliar brand should work. I don't use any of the especially fast acting analogs, just plain insulin. Get your baseline, inject IP and begin collecting your time points.

The original question was what do we have to monitor with high statin therapy. If we use other therapies may other metabolic Parameters would also have to be considered. In statin therapy I would monitor lipids, glucose and HbA1c, ALAT, may be  CK (at least at the beginning) and eventually hsCRP.

Bile malabsorption can also increase serum triglyceride levels, while decreasing the cholesterol pool. This might be an autoimmune phenomenon, but I'd love to hear anyone's thoughts on the matter. And yes, these changes may be transient.

Thank you Sir...

Thank you sir,

But, you can send any research articles which followed this type of  protocols for serum.

Insulin resistance prevalence is very high among patients with NASH (60-85%). In fact it is pathophysiologically implicated in NAFLD in most of patients. None less, not all patients with NASH have insulin resistance. In the other hand, insulin resistance and DM are detected in 17 – 35% of patients with chronic hepatitis C. The mechanisms by which HCV produces insulin resistance and DM are not clearly known.  It was observed that HCV induces insulin resistance regardless of body mass index and fibrosis stage. In a study conducted in a transgenic animal model, the HCV core protein was able to induce insulin resistance, steatosis and DM. In addition, insulin resistance induces antiviral treatment resistance in HCV patients and it is associated to in increments of mortality. I attached one publication that can be of help in this field.

 Liver cirrhosis and diabetes: Risk factors, pathophysiology,clinical implications and management. World J Gastroenterol 2009;15:280.

jejuno-ileal Bypass was practiced for Hypercholesterlemia also .It very effectively cures the problem but adds several other problems including fractures due to severe malabsorption,hence this is not being practiced.I had an opportunity to reverse one.

Vijayendra:

Glad to help. Fenugreek is a good choice, but just here are a few tips culled from review:

(1) Only trials that administered Fenugreek seed powder in upper dose range (>= 5g) achieved a significant reduction in glucose parameters to a clinically releevant degree;

(2) Low doses (< 2 g) of hydro-alcoholic extracts were ineffective;

(3) The upper dose range that includes doses from 5 - 25 g of fenugreek seed powder provided an additional benefit, of also lowering postprandial glucose levels, again to a clinically releevant degree; this was true of fenugreek raw seeds, extracted seed powder, cooked seeds (dosed at 25 g) and gum isolate of seeds (dosed at 5 g) while degummed seeds (even up to 25 g) had negligible effect.

Sialic acid

I do not think is because reduced carnitine availability.

The combined metabolic derangements seen in MADD are all due to deficient activity Electron Transfer Flavoprotein (ETF) and/or its electron transfer flavoprotein:ubiquinone oxidoreductase ( ETF: QO) which impairs all FAD-dependent dehydrogenases .

Glutaric acid accumulates as a result of deficient Glutaryl-CoA dehydrogenase (FAD-dependent enzyme ) and reduced carnitine availability is secondary to accumulation of short- and medium-chain acylcarnitines due to impaired acyl-coenzyme A dehydrogenases (FAD-dependent enzymes ).

Note : Some MADD patients had normal ETF and ETF-QO activity, suggesting other unknown disease mechanisms.

Metabolic syndrome is characterized by cardiometabolic risk factors that include obesity, insulin resistance, hypertension and dyslipidemia. Oxidative stress is known to play a major role in the pathogenesis of metabolic syndrome. The objective of this study was to examine the effectiveness of hydrogen rich water (1.5-2 L/day) in an open label, 8-week study on 20 subjects with potential metabolic syndrome. Hydrogen rich water was produced, by placing a metallic magnesium stick into drinking water (hydrogen concentration; 0.55-0.65 mM), by the following chemical reaction; Mg + 2H(2)O --> Mg (OH)(2) + H(2). The consumption of hydrogen rich water for 8 weeks resulted in a 39% increase (p<0.05) in antioxidant enzyme superoxide dismutase (SOD) and a 43% decrease (p<0.05) in thiobarbituric acid reactive substances (TBARS) in urine. Further, subjects demonstrated an 8% increase in high density lipoprotein (HDL)-cholesterol and a 13% decrease in total cholesterol/HDL-cholesterol from baseline to week 4. There was no change in fasting glucose levels during the 8 week study. In conclusion, drinking hydrogen rich water represents a potentially novel therapeutic and preventive strategy for metabolic syndrome. The portable magnesium stick was a safe, easy and effective method of delivering hydrogen rich water for daily consumption by participants in the study.

PMID:

20216947

[PubMed]

PMCID:

PMC2831093

Free PMC Article

Vitamin B 12 level was not measured (low-Resource setting).However she is having B 12 one mg intramuscular every 7days. Tiglylglycine, and propionylglycine were not measured.