Metabolic Syndrome
Metabolic Syndrome - Related Videos
05:41
Metabolic Profile Analysis of Zebrafish Embryos
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Cited by 42 •
2013
Zebrafish represent a powerful vertebrate model that has been under-utilised for metabolic studies. Here we describe a rapid way to measure the in vivo metabolic profile of developing zebrafish that allows the comparison of different mitochondrial function parameters between genetically or pharmacologically manipulated embryos, thereby increasing the applicability of this organism.
00:52
What is Metabolism?
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2019
Overview Metabolism represents all of the chemical activity in a cell, including reactions that build molecules (anabolism) and those that break molecules down (catabolism). Anabolic reactions require energy, whereas catabolic reactions provide it. Thus, metabolism describes how cells transform energy through a variety of chemical reactions, which are often made more efficient with the help of enzymes. Metabolism Is the Sum of All of the Chemical Reactions That Take Place in an Organism
08:31
Conscious and Non-conscious Representations of Emotional Faces in Asperger's Syndrome
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Cited by 5 •
2016
An EEG experimental protocol is designed to clarify the interplay between conscious and non-conscious representations of emotional faces in patients with Asperger's syndrome. The technique suggests that patients with Asperger's syndrome have deficits in non-conscious representation of emotional faces, but have comparable performance in conscious representation with healthy controls.
10:19
An Introduction to Cell Metabolism
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2023
In cells, critical molecules are either built by joining together individual units like amino acids or nucleotides, or broken down into smaller components. Respectively, the reactions responsible for this are referred to as anabolic and catabolic. These reactions require or produce energy typically in the form of a “high-energy” molecule called ATP. Together, these processes make up “Cell Metabolism,” and are hallmarks of healthy, living cells.JoVE’s introduction to cell metabolism briefly...
10:31
An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
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Cited by 12 •
2018
We describe methods to develop an experimental model of diet-induced metabolic syndrome (MetS) in rabbits using a high-fat, high-sucrose diet. Animals developed central obesity, mild hypertension, pre-diabetes, and dyslipidemia, thus reproducing the main components of human MetS. This chronic model will allow acquisition of knowledge underlying mechanisms of disease progression.
FAQs
Insulin resistance acts as a central metabolic disturbance that links several disease processes. When cells respond poorly to insulin, blood glucose can rise, lipid metabolism becomes abnormal, and inflammatory and vascular changes may develop. These interconnected effects help explain why treatment must address more than glucose alone and why progression can increase cardiometabolic risk.
Inflammation and vascular dysfunction extend the consequences of metabolic imbalance beyond abnormal laboratory measurements. They represent biological pathways through which insulin resistance, altered lipids, and elevated blood pressure can contribute to cardiovascular risk. Recognizing these links supports an integrated treatment strategy rather than managing each abnormality as an entirely separate problem.
Drug selection can be organized according to the dominant pathway or risk factor: glucose-lowering therapies address abnormal blood glucose, lipid-lowering therapies target triglyceride and HDL-related disturbances, antihypertensive therapies address elevated blood pressure, and weight-management therapies target excess weight. This framework encourages complementary treatment decisions while preserving attention to the patient’s combined risk profile.
Insulin resistance provides a mechanistic rationale for combining interventions that influence glucose, lipid metabolism, body weight, inflammation, or vascular function. Focusing only on one measurement may leave related abnormalities insufficiently addressed. In pharmacology, identifying this underlying process helps connect treatment selection with the broader pattern of metabolic and cardiovascular risk.
Lifestyle modification should accompany pharmacological treatment because the syndrome reflects interconnected metabolic and cardiovascular disturbances rather than a single isolated target. Medication can address specific abnormalities, while lifestyle measures support the broader management strategy. Using both approaches helps create an integrated plan aimed at preventing progression and reducing associated complications.
A multi-target approach is relevant when several abnormalities contribute to a patient’s overall risk. Glucose-lowering, lipid-lowering, antihypertensive, and weight-management therapies each address different components or pathways. Their coordinated selection supports rational drug use, particularly when management must address abnormal glucose, blood pressure, lipid metabolism, and excess weight together.
Management aims to reduce the likelihood that interconnected metabolic abnormalities will progress to cardiovascular disease or type 2 diabetes. Risk assessment helps identify the relevant treatment targets, while rational drug selection addresses the contributing pathways. The desired outcome is not merely improvement in one measurement, but prevention of broader complications through coordinated care.