- Kulvinder kochar kaur added an answer:15Why metformin (glucophage) causes weight loss and reduced appetite despite stimulating AMPK?
5' AMP-activated protein kinase or AMPK has been found to stimulate appetite and cause weight gain in experimental rats. Metformin acts by stimulating AMPK but which leads to weight loss in patients treated with Glucophage. What's the confounding reason?
Role of AMP-activated protein kinase in mechanism of metformin action
Although i rodent models metformin is associated with weight loss no consistent weight loss effect has been noticed in human stidies-in fact in a review on obeze infertile males there were no conclusive evidence tha just by themselvs metformin is useful for getting fertility restored in obese males and yes the effect on hypothalamus and liver counts and what dosage it is tolerated -in fact it is much more convenient to use glp1 agonists like liraglutide in such patients which not only helps to reduce hba1c levels but is associated with remarkable weight loss irrespective of diabetic status or not in the obese psrson .Following
- David Jacobi added an answer:3What is the most economical and feasible way to measure GLUT4 transporter in rats muscle?
Molecular biology, metabolism, insulin resistance, metabolic syndrome, obesity, diabetes, cellular signalling
You can do the following:
- gene expression (mRNA) on skeletal muscle homogenates
- Western blot with anti GLUT4 antibody on skeletal muscle homogenates
- glucose uptake ex vivo on muscle fibersFollowing
- Yi-hsieng Samuel Wu added an answer:4How does the level of serum albumin change during the development of the metabolic syndrome?
I'm interesting how may change level of serum albumin when we have obesity and NAFLD also with metabolic syndrome.
In addition, metabolic syndrome is not equal to the NASH or NAFLD. All cases I provided are based on hepatological investigations, so you may have to search other case reports of DM, obesity, etc.Following
- Abdul Hafeez Kandhro added an answer:3Are there any methods for reducing SREBP2 gene in hypercholesterolemic patients?
Cholesterol homeostasis is crucial for cellular function and organismal health. The key regulator for the cholesterol biosynthesis is sterol-regulatory element binding protein (SREBP)-2. There are many research articles on inhibition of SREBP2 gene but, still mysterious mechanism which could be maintained or controlled to reduce cholesterol level and prevent coronary diseases and metabolic syndrome.
not meaningful answers,,,,,,Following
- Alexandr Rumyantsev added an answer:10What is the best diagnostic criteria for metabolic syndrome in adults?
I'm researching about the prevalence of metabolic syndrome in a population of adults, for my dissertation. We have many cutoff points for the diagnosis of the syndrome, but what would be the best for use in epidemiological studies? It would be interesting to make a comparison between two or more diagnostic criteria?
What do you think?
Thank you, already!
The syndrome is called "metabolic syndrome", so the most important criteria are the HOMA index, waist/hip ratio, concentration of triglycerides. Choice of 3 components from five in consensus confusing in research. To determine if the elephant would have to choose 3 of the five signs it is unknown what the animals were housed in different zoos around the world. And still another sign would have recognized the chief. Without insulin resistance won't make sense to talk about metabolic syndrome. In my opinion, metabolic syndrome is the "diabetes mellitus type III".
But the diagnostic criteria for metabolic syndrome in adults at International Diabetes Federation (IDF) has greater sensitivity.Following
- Yves Van Assche added an answer:8How can I solve a metabolic syndrome problem?
Could animal husbandry science have a role with this case?
Amazing but true!
According to Low Urine pH: A Novel Feature of Metabolic Syndrome, A difference of less than 1pH in your urine may determine whether or not you will suffer from the symptoms of metabolic syndrome! "Participants with the metabolic syndrome had a significantly lower 24-h urine pH compared with participants without the metabolic syndrome. Mean 24-h urine pH, adjusted for age, gender, creatinine clearance, and 24-h urine sulfate, decreased from 6.15, 6.10, 5.99, 5.85, to 5.69 with increasing number of metabolic syndrome abnormalities". - (2007 Maalouf, et al pg 1, paragraph 3) If you think you may be affected by metabolic syndrome, talk to your doctor.Following
- Mohammad Ishraq Zafar added an answer:7Is anyone aware of studies that have been examining the relationship between subclinical hypothyroidism and central obesity or hyperglycemia?
We are studying the relationship between subclinical hypothyroidism and metabolic syndrome components and would like to know if there are other studies investigating the risk of central obesity or hyperglycemia in subclinical hypothyroidism in general population.
Please check the following links, may be it is useful for your study.
- Abu-Eid I Sameer added an answer:11Is impaired insulin secretion a risk factor for CVD?
Insulin resistance is a key component of the metabolic syndrome well known to drive the risk of CVD. Does the impairment of insulin secretion, in the absence of insulin resistance, contribute to increased risk of CVD?
Theoretically yes, but you need to prove it experimentally.Following
- Silvia Clapauch added an answer:11Do you agree that METS is a multifactorial disease which involves neuro, endocrine,immune and metabolic systems?I am interested in clarifying pathogenetic mechanisms of METS
By non-metabolic aspects of metabolic syndrome I meant that metabolic syndrome has non-metabolic comorbidy such as: (i) cardiovascular ischemic disease (insulin, increasing PAI-1 levels prevents blood clots from being dissolved), (ii) thromboembolic events (the same), (iii) female reproductive disorders, such as PCOS, first trimester losses, pre-eclampsia, eclampsia (elevated PAI-1 levels prevent matrix metalloproteinases from being activated, which prevents ovary remodeling and impairs placentation), (iv) male reproductive disorders, especially erectile dysfunction, (v) mental disorders such as depression (elevated PAI-1 levels prevents appropriate NMDA receptor activation; it also prevents proneurotrophins from being cleaved into mature, antiapoptotic neurotrophins, (vi) osteoarticular problems related to both osteopenia and excessive weight, the list is vast.
I totally agree that there are lots of gaps. Nonetheless, I guess it is time to reunite all non-metabolic comorbidity of MetS under a big umbrella, and the most important: it is it time to focus on complications derived from hyperinsulinemia in patients who are not overweight or obese.
- Ruby Red added an answer:7Curious about your main assumption regarding high-fat diets: Is there significant evidence that you could cite that supports your claims?The premise at the top of your study, "Consumption of high-fat foods is one of the major causes of obesity," seems to me to be something that's been up for debate for some number of years now, with people actually losing weight on high-fat/low-carb diets. Is there significant evidence that you could cite that supports this claim? If this is your assumption on the outset, doesn't that naturally skew the parameters of the study?
Aren't many obese people who consume high amounts of fat also impacted by other factors, such as thyroid disruptors in the environment; the excess of omega-6 oils in most packaged foods, high-carb + high fat diets, and sedentary work in temperature controlled environments?
I presume you're addressing me, as there's no one named Rudy in this thread.
Are you aware of how fat impacts insulin response compared to carbohydrate consumption? Your logic is overly simplistic. Furthermore, I don't see your name on this paper, so why do you have so much skin in game?
Unfortunately, the "high fat" or "high carb" diets fed to lab rats are often not strictly one macronutrient, and sometimes these diets are measured as a percentage of calories consumed, as opposed to a specific calorie count. A diet high in carbs and fats has very different effects than a diet that is strictly fat or a high protein+fat diet.
I contend that not enough studies have been done with other diet formulations and that the assumption regarding fat and weight gain is still very much that.
It's possible to make anyone obese with too much of a macronutrient. Heck, alcohol offers 7 calories per gram, so why not feed rats a high alcohol diet and see how that impacts obesity?Following
- Gary Robert Gaffney added an answer:3Does anyone have contemporary research linking atypical antipsychotics to iatrogenic outcomes?
There have been a variety of hypotheses relating to the biological and iatrogenic causes of metabolic syndrome in regard to mental illness experienced by individuals diagnosed with a mental disorder. I am interested in researching iatrogenic outcomes linking atypical antipsychotics with metabolic syndromes.
You are talking about the disturbed metabolic states in patients treated with neuroleptics..like glucose intolerance and insulin abnormalities. Check out Chadi Calage's work, he has published in that exact area.Following
- Emiliano Schena added an answer:2Does anyone have a good reference that describes how to calculate the error propagation in measuring VO2 using a metabolic cart (e.g., ParvoMedics)?
I always have students calibrate the various components of our metabolic cart (e.g., mass air flow meter, O2 analyzer, CO2 analyzer). However, I am not sure what the total error of measurement is for final measurements such as VO2, VCO2, R, etc. I'd like to present a method to my students that would allow them to calculate the propagation of error for any complex measurement they might make in lab.
In the following paper a calibration methodology for metabolic analyzer and the estimation of uncetainty have been described.
- Mirshd Puthanveettil added an answer:7Is there somebody who has used Lipoprotein associated phospholipase A2 as a marker to assess the cardiovascular risk?
I am doing a work on Metabolic syndrome and would like to use Lipoprotein associated phospholipase A2 as a marker to assess the cardiovascular risks. I would like to know the details.
Thank you MargarethaFollowing
- Prof. Ashraf Mahdy Sharoba added an answer:5Can we use the biomass ( fresh spirulina) in production of industrial foods enriched with spirulina? What foods or drinks ?
I woud like to use food products enriched with spirulina platensis for patients with diabetes, metabolic syndrom and etc so that each patient intake 5 to 6 gr or more spirulina daily .I think vegetable puree is suitable
We use the spirulina in the manufacture of juices and snacks, biscuits and baby foodFollowing
- Zheng Jiawen added an answer:6Is there any method possible to evaluate the oxidation rate of palmitate without using a radioisotope?
I'm going to measure the oxidation rate of palmitate in vitro by using a skeletal muscle model with C2C12 cell. I have read many papers but yet have not been able to find out a suitable method avoid using radioisotope 14C. Is there any possible method available.
Appreciate any respond.
Thanks everyone who gave advice to me. For Dr. Martin, the reason why I avoid using 14C is the same as Jana. Our lab is not qualified of using radioisotope, neither do we have the machine. I have found out other lab holding a O2 electrode and maybe I'll try the method. Thanks very much!Following
- Priyathama Vellanki added an answer:11How can I analyze variables with several zeros?
Are non-parametric tools sufficient to handle properly these kind of data? Is there any transformation I could apply in order to "normalize" distribution?
Thanks in advance
I agree with the explanation by Dr. Herraiz. Another alternative we have done is to add 1 to all the data points of that variable so you can perform a log transformation. For example if your data is 0,0,2,3,5, you can now make them 1,1,3,4,6. Or you can also perform non-parametric tests.Following
- Rejina Kamrul added an answer:5What are the most reliable measures (indicators) of treatment adherence in metabolic syndrome?We are looking at predicting adherence to medical and behavioral health care recommendations among individuals with metabolic syndrome. I'm curious if anyone might be able to provide personal insight into specific indicators (behavioral or otherwise) that have been effective/reliable in quantifying the construct of treatment adherence?
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.caFollowing
- Jan Azarov added an answer:4Could anybody advise what is the cost for the high fat (or high carb) diet for rabbits per day?
I am planning the next step of my research from experimental type 1 DM to obesity/metabolical syndrome/type 2 DM. I try to estimate the potential expenses. There is a good deal of information on the web sites concerning the scientific aspects of research diets; suprisingly, I could not figure out the pricings. Does anybody have the experience or suggest some clear price list? Thank you very much in advance.
Thank you very much! Very useful.Following
- Dumitru Branisteanu added an answer:3Is it possible that the level of FSH is higher but the level of testosterone and LH is lower in plasma?Need explanation regarding this condition in male.
Depends of the situation and hormone levels. As written above, testosterone secretion depends of LH and not FSH. Autoimmune hyophysitis may for instance evoluate insidiously and selectively on certain, but not all pituicites, for instance causing selective LH, but not FSH deficiency and, consequently, causing a decrease in testosterone secretion.Following
- Frank Wagener added an answer:3Does anyone having protocols for assessments of IL-1b, IL-6, IL-10 and IL-18 for in vivo and in vitro metabolic syndromes research?
Cytokines involved in endothelial dysfunctions.
most stimple is cytokine beads array using flow cytometryFollowing
- Christelle Douillet added an answer:14Is HOMA-IR valid as a proxy measure of insulin resistance in animal models?
A large number of murine studies report HOMA-IR alongside IPGTT/OGTT and fasting glucose/insulin levels as a proxy of systemic insulin resistance. However, is this a valid approach? How applicable is the HOMA-IR calculation to murine physiology?
I find interesting the answer of Vincent Blok and his team's paper (Van Dijk et al, Lab Anim 2013) regarding 14.1 factor for mice instead of 22.5. However, what is proper conversion factor for mouse insulin in ng/mL into mU/L? I understand that IU had been defined for human insulin (26 IU/mg) but not for mouse insulin. Is that factor of 26 IU/mg acceptable for converting mouse insulin mg into IU ?Following
- Timothy Graham added an answer:12Can we use glucose levels and lipid profile levels obtained from non-fasting blood to identify metabolic syndrome in children and adolescents ?
Metabolic syndrome in children and adolescents
Possibly... most non-fasting samples will not have been obtained in the immediate post-prandial state, which helps -- takes people time to get to an office or phlebotomist etc to get the blood drawn, and most of them aren't eating actively up to the point their blood is drawn. In addition, 1 hr post-prandial values should still normally be less than 170 mg/dL. If you have some certainty that the patients have been sampled more than 1 hr after their last meal, you could use an even more stringent cut-off value of 155 mg/dL for diagnosing "dysglycemia". This is not ideal, but doable if you have no other options. For metabolic syndrome, you might be able to focus on Triglyceride:HDL ratio to improve predictive value a bit.. Triglycerides are more problematic because they can remain elevated for up to 6-7 hrs after a meal. They tend to peak at about 4 hrs post-prandially, usually at about 2-3x above fasting values. In randomly collected samples, this means you are practically guaranteed to pick up some degree of prandial triglyceride elevation. Even so, you could conceivably come up with a conservative cut-off value that will only pick up individuals with triglyceride levels much higher than what you would call normal in fasted or 4 hr post-prandial children/adolescents. None of these are ideal fixes, but if you are stuck with random non-fasting samples, and your number of samples/subjects is sufficiently high, then you might be able to come up with some rationale models that could reasonably be expected to identify individuals with MetSyn.Following
- Vincent Bloks added an answer:7Is there any equation for calculating fat and carbohydrate oxidation in mice?Most papers use Peronnet and Massicotte, 1991, which is based on human values. I'm wanting to find an equation that is more suitable for mice models.
Perhaps the formulae we used in this paper will helpFollowing
- Andy Biddulph added an answer:10Is obesity as an autoimmune disease?What do others think?
Fei and Zhao in a paper in Nature showed that morbid obesity was the result of a large population of Klebsiella mobilis (only they used the old name which I can't remember) in the gut. They cured the problem by giving a diet of whole grain and Chinese medicinal vegetables which reduced the K mobilis population to normal levels. Some obesity is clearly an actual disease.Following
- H. Ram added an answer:4Which protocols are used for antioxidants activity measurements from serum and animal tissue?For free radicals activities directly affected in metabolic syndromes.
Thank you sir,
But, you can send any research articles which followed this type of protocols for serum.Following
- Roldan de Guia added an answer:6What is the best resource for identifying/visualising gene regulatory pathways?
I'm looking for an open source resource for visualising known gene/protein regulatory pathways, principally for innate immune system activation involved in obesity and the downstream responses, but also for other pathways involved in obesity/metabolic syndrome (if these broad maps exist!).
Can anyone point me in any directions?
- Vincent Bloks added an answer:3Does anyone find accumulation of big lipid droplets in HCC?I found some big lipid droplets in the murine model of HCC.
Do they arise from the experimental methods ,or it is the normal phenomenon in the tumorigenesis of HCC?
Hi, perhaps this disscusion will helpFollowing
- Monica Cavali added an answer:10Is fasting sugar along with blood pressure and waist circumference a cost effective way of screening metabolic syndrome?
Various definitions and criteria used to diagnose metabolic syndrome. Its a common observation that central obesity, high blood pressure and impaired fasting sugars are an important triad. So I propose fasting blood sugar as a single blood test to identify metabolic syndrome in poor resource setting.
I would like to remember that in chidren glycemia usually is normal, it's better to use insulin or insulin resistance .Following
About Metabolic Syndrome
Focused on understanding the molecular mechanisms of metabolic syndrome