- Nadia Rezaei added an answer:Can 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
Dear Puganeswary Sukumaran
Thank you very much.Following
- Carlos Guijarro Herraiz added an answer:How 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
As an alternative, a variable equal to zero may be considered as essentially equal to a very low value. E.g. increase in body wieght as 0 kg is essentially equivalent to increase in 1 gram. According to the parameter, this minimal irrelevant value may be substitued for zero allowing for logarithmic transformation.Following
- Do 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
thanks for your question that is, for me, crucial for the research, to face damages of uncontrolled inflammatory deseases such that occour in cancer,obesity. diabetes,HIV-patients threated with HAARTand cardio-vascular and neurological deseases.
I believe that the pathogenesys of the metabolic diseases is much clearer now as our knowledge of adaptive systems is increased:however the complexity of the systems is very high, as expected, and the threatment will be complex and multi -targeted.it can't be excluded that an herbal formulation will be active.Following
- Apurva Kumar added an answer:Is 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?
Yes, mainly due to its simplicity. Probably Matsuda index would be better.Following
- Timothy Graham added an answer:Can 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:Is 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:Is 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:Which 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
- Ruby Red added an answer:Curious 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?
That's not evidence based on rigorous science. That's calories in = calories out math and anyone who spends any time studying human physiology knows that it's not a zero sum game. Hormonal cascades, gut bacteria, immune responses to specific types of nutrients all impact how a body stores or burns fat. If that equation worked so simply, the "low-fat = fat loss" solution would be available to all, but it's not. What about epileptics who are on high-fat diets, but aren't obese?Following
- Roldan de Guia added an answer:What 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:Does 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
- Sheikh Mohammed Shariful Islam added an answer:What 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?
We used Morisky's 8 scale medication adherence tool to measure adherence among patients with type 2 diabetes in Bangladesh. It is a easy tool to use in clinical and research settings.Following
- Monica Cavali added an answer:Is 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
- Sherif Wagih Mansour added an answer:Which method is recommended for determining body fat content of patients in a clinical trial?Of course, the method should be fast, inexpensive and harmless for the probands. However, I am in doubt, if measurement results of commercially available body-fat scales have sufficient correctness and precision. If they have, are normal scales from the local supermarket sufficient or do they need more bells and whistles?
BMI calculation with axillary skin fold in addition to waist/Hip circumferenceFollowing
- Victor Maduabuchi Oguoma added an answer:Waist Circumference cut point for sub-Saharan Africans?
What are the best ways to develop the Waist Circumference cut point for sub-Saharan Africans? I understand that the current clinical definition of obesity for sub-Saharan Africa according to the IDF is by using the European Waist Circumference cut point.
Thanks heaps for your detailed response and suggestion.
- Ali Abdil Razzaq Muhammed Noori Aldallal added an answer:What the role of leptin in the pathogenesis of diabetes?Especially in obese persons?
The adipocyte hormone leptin acts mainly via central mechanisms to reduce food intake and increase metabolic energy expenditure. Although leptin concentrations may increase in obesity this tends to be associated with the development of leptin resistance which appears to reduce its effectiveness. Leptin may act on skeletal muscle to improve insulin action possibly via activation of AMPK and increased fatty acid oxidation suggesting that it probably does not play a significant role in insulin resistance.For more please read at following link and papers attached.
with my best regardsFollowing
- Hila Roshanravan added an answer:Will TNFα induce the same type of stress in the presence of serum?Will TNFa induce the same degree of stress when I differentiate the cells in the absents or presents of serum?
Usually to induce an effect, TNF alpha is used along with Serum-free mediaFollowing
- Anu Makela added an answer:When Byetta breaks bad?Recently I have had 2 patients successfully treated with Byetta for 18 months that suddenly became ill without any abnormal pathology or abnormal scans.
They have both proceeded to insulin and are now requiring up to 200 units a day U500 INSULIN. Has anyone had a similar experience and any thoughts behind why?Apparently with merely increasing insulin production with Byetta, they finally developed a higher level of insulin resistance. Did you try any insulin receptor sensitizers (Metformin or Actos)? Type 2 diabetics generally develop insulin resistance quite quickly if they are not placed on a medium low carbohydrate diet along with adjusted medication levels. Insulin receptors are also senditive to changes in lipid raft constructs ie. Changes in chloesterol levels ( very high or too low). Another possibility is adevirus infection. Adenovirus is known to increase up to fourfold the secretion of PC-1 which is an insulin receptor inhibitor. In this case biguanidine (again Metformin) will decrease PC-1 activity, or if your patients are also anemic, a two month treatment with EPO has been known to return PC-1 levels back to normal limits. Hope this gives you something to go on...Following
- Michelle Tegg added an answer:Insulin degrading enzyme (IDE) activity quantification?Is there anyone that knows a method or a protocol to correctly quantify the activity of IDE? I usually used a ELISA kit but unfortunately the kit was discontinued and I can't find any alternative.Apologies, for some reason ResearchGate didn't notify me of these answers, and only just saw them. If you are having difficulties with this protocol, may I suggest that you try the adaptations that are mentioned in the below publication? Hopefully it may be of some help, I had success with this protocol. Good luck!Following
- Anil Kumar Pandey added an answer:Can the cut off of epicardial fat can be a diagnostic criterion of metabolic syndrome and coronary artery disease?Measuring the amount of epicardial adipose tissue (EAT) can be a novel parameter that is inexpensive and easy to obtain and may be helpful in cardiovascular risk stratification. However, the relationship between epicardial fat and cardiac function and that between epicardial fat and cardiac risk factors is less well described.Visceral adiposity is a marker of increased risk but not readily assessed and may be costly to measure. Epicardial fat thickness is associated with cardiac morphologic abnormalities on echocardiography. This may be a more sensitive assessment of body fat distribution. It is easily available at echocardiography and simple to acquire at no added cost and training. However standardization of measurement and sensitivity of epicardial fat thickness in predicting CV risk are needed. Comparison of this simple and inexpensive measure with waist-hip ratio, BMI, Dexa scan of visceral fat, and MRI of visceral fat are needed.Following
- Closed account added an answer:Are non-adherent people with Celiac Disease more likely to develop metabolic syndrome?Recent studies have shown that there is a high percentage of people who are overweight or obese at the time of diagnosis. Celiac patients have a higher risk of autoimmune diseases, including diabetes.Francisco, how were these patients followed for gluten-free diet compliance? That could be a factor.Following
- Do you believe that cortisol and its receptor have a key role in the metabolic syndrome? Is it a good basis to open a debate on the pathogenesis of the metabolic syndrome?Obesity and other chronic inflammatory diseases are associated with normal or slightly modified plasma levels of cortisol, which are considered insufficient to explain signs and symptoms of chronic inflammation. However increased cncentrations of cortisol in liver and fat cells caused by activation of 11Beta HSD-1 by inflamatory diseases may greatly contribute to abnormalities of the metabolic syndrome including obesity, insulin resistance, hyperinsulinemia , dyslipidemia, increased fat deposit, near inflammed tissues, hypoandrogenaemia, mild hypercortisolemia, anaemia , osteopenia and activation of the sympatetic system related to chronic inflammation.Following
- Turgay Celik added an answer:What is the impact of metabolic syndrome (MS) on long-term clinical outcomes in patients with (NSTEMI) or unstable angina pectoris (USAP)?In acute coronary syndrome (ACS) patients, those with MS were more likely to be female, have a history of percutaneous coronary intervention, and have a lower left ventricular ejection fraction and higher Thrombolysis in Myocardial Infarction (TIMI) score. Since the MS has a negative long-term impact on cardiovascular mortality and reinfarction in patients with ACS, it can be used as a marker of cardiovascular mortality in patients with ACS and aggressively targeted.
The patients with metabolic syndrome undergoing primary PCI experienced poor myocardial perfusion grades after intervention.please see our Groups study published in Coronary artery disease.Following
- Khaled Saad added an answer:Could mast cell stabilizer be an adjuvant therapy in type-2 diabetes?See aboveShi, Michael A., and Guo-Ping Shi. 2012. Different roles of mast cells in obesity and diabetes: Lessons from experimental animals and humans. Frontiers in Immunology 3:7.
- Barak Rotblat added an answer:What can be used as a marker for oxidative damage analysis in samples that will be frozen for over a year?We would like to analyse oxidative damage in the tissue of mice. Could you suggest a marker which would remain stable in samples frozen in -80°C for a year or even more? Obviously, enzyme activities or TBars are not an option, as they degrade after a month or so, but what about some DNA modifications, etc? Do you have any experience with this? Thanks a lot!You can fix you samples in PFA, mount and using standard IHC, stain with anti–8-oxo-dGuo that marks oxidized DNA. You will see the brown stain particularly in the nucleus of cells that suffer from high oxidative damage. This can compliment what Rajesh was suggesting, using carbonylated protein assay to analyse lysets. There is a nice kit from Cayman chemicals.
- Alain Aubourg added an answer:Anyone know a good model to induce hypothalamic inflammation?I am looking for models to induce hypothalamic inflammation in mice.
The most common model is through high-fat diet administration, but I'm looking for something related to TNF-alpha or other cytokines (intracerebroventricular).
Does anyone know or have used another induction model?Hypothalamic Inflammation: Marker or Mechanism of Obesity Pathogenesis?Joshua P. Thaler , Stephan J. Guyenet , Mauricio D. Dorfman , Brent E. Wisse et Michael W. Schwartz ⇑Following
- Do you believe that cortisol and its receptors have a key role in the metabolic syndrome? Is it a good basis to open a debate on the pathogenesis of the metabolic syndrome ?I agree with Rajesh Parsanathan, and Dipti Sarma. In METS we are faced with an extremely complex system resulting from interaction, at least, of cortisol, mineralcorticoids, sex steroids hormons and, of course, the immune system. In this integrated system the weak side is metabolism ( hyperglicemia,dyslipidemia, etc.), but when we recognize METS by its metabolic symptoms is late, then we have to find other markers of disease ( endocrine or immune) to allow prevention, but this is also difficult. In other words we can't cope METS without taking into consideration all systems involved. To continue discussIon , see my last paper full text .Following
About Metabolic Syndrome
Focused on understanding the molecular mechanisms of metabolic syndrome