Dangers of Weightloss Drugs Discussion.
The Dangers of a Weight Loss Drug
by Libertas AcademicaOpens in a new window
For this discussion we will use another case study from the National Center for Case Study Teaching in Science (NCCSTS) from the University at Buffalo. This case study explores the order and linkage of the biochemical processes involved in ATP synthesis in mitochondria (glycolysis, TCA cycle, electron transport chain, proton pumping, ATP synthase activity) and discusses how mitochondria may generate heat to maintain body temperature.
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Click the link for a PDF interrupted case study about the dangers of a weight-loss drugOpens in a new window.
As your read through the case study consider the following questions:
What are the consequences of a proton gradient and how could a gradient be used in the mitochondrion?
What must be an important characteristic of the inner membrane in order for this gradient to be established and maintained?
If you “poke a hole” in the inner membrane such that protons can freely move across it, what would happen:
To the proton distribution across the inner membrane?
To the amount of ATP produced by the mitochondria?
To the energy released in the movement of the protons?
Most ATP is consumed soon after its production. The cell has ways of detecting how much ATP is produced and needs to keep its supply constant. If you poke a hole through the inner membrane, what might the cell do to try to adapt to the change and reestablish previous levels of ATP? List all the possibilities.
What are the physiological effects that DNP has on the body (list as many as possible). Which of these effects are energy-related? Which linked processes do you think DNP is uncoupling taking into account the physiological effects you listed in Question 9?
Considering what you know about coupling, what would the effects be of blocking electron transport at each complex?
Submit an original post based on the following questions:
Based on your understanding of the mechanism of action of DNP, how dangerous do you think DNP really is? For an athlete, what are the consequences of ATP depletion? Should Connor take DNP to lose weight?
Defects in electron transport and oxidative phosphorylation are responsible for a myriad of symptoms and diseases. The genetics of mitochondrial disease are complex due to the fact that mitochondrial proteins are encoded both by nuclear and mitochondrial DNA. Because mitochondria vary in number and in importance in different tissues, the outward symptoms are also complex and difficult to diagnose. The Online Mendelian Inheritance in Man® (OMIM®) is a comprehensive, authoritative compendium of human genes and genetic phenotypes that is freely available and updated daily. The full-text, referenced overviews in OMIM contain information on all known Mendelian disorders and over 12,000 genes. Go to Online Mendelian Inheritance in ManOpens in a new window and perform a search of mitochondrial diseases. Select one that you find interesting. What is the molecular basis of the disease you selected? What are the symptoms? Knowing what you know now about mitochondria, transport, and respiration, explain how the defect might affect respiration. Can you suggest a possible therapy for this disease?
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Dangers of Weight Loss Drugs.
Risks of a Weight Loss Drug
Academica Libertas
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This discussion will employ a case study from the University at Buffalo’s National Center for Case Study Teaching in Science (NCCSTS). This case study discusses how mitochondria generate heat to keep the body warm (glycolysis, TCA cycle, electron transport chain, proton pumping, ATP synthase activity).
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Click here for a PDF case study on a weight-loss drug’s hazards.
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As you read the case study, ponder the following:
How could a proton gradient be used in the mitochondrion?
What inner membrane property is required to produce and maintain this gradient?
A hole in the inner membrane allows protons to freely travel across it.
To the inner membrane proton distribution?
To the mitochondrial ATP production?
To the protons’ movement’s energy?
Most ATP is used up quickly. The cell can detect how much ATP is produced and must maintain a consistent supply. What happens if you pierce the inner membrane and try to restore ATP levels? Make a list of options.
What are DNP’s physiological effects? (list as many as possible). Which of these is an energy effect? Given the physiological impacts stated in Question 9, which connected processes do you think DNP is uncoupling?
What would happen if you stopped electron transfer at each complex?
Answer the following questions in your post:
How harmful do you think DNP is based on your knowledge of its mechanism of action? What are the effects of ATP depletion on athletes? Should Connor take DNP?
