Diabetes : Diabetes, Type I And Type II Essay

Diabetes : Diabetes, Type I And Type II Essay

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Diabetes first appeared millennia ago and given its name meaning “a siphon” – referring to the excessive diuresis associated with the ailment7. Diabetes was further classified into “insipidus” and “mellitus” which distinguishes between the absence and presence of sugar, respectively, and now diabetes mellitus is colloquially referred to as diabetes. Though present throughout the centuries, the illness now presents a major health threat to upwards of 300 million people worldwide – and growing8.
There are two sub distinctions of diabetes mellitus, type I and type II. Type I results from pancreatic beta cells being unable to produce insulin1. Type II occurs when cells become desensitized to blood glucose levels and require greater amounts of insulin for the same glucose uptake1. Cell desensitization in the liver also prevents glycogen containing cells from recognizing inhibitory insulin signaling resulting in glucose release to the blood which raises blood glucose levels9. The pancreas cannot compensate for these additional insulin requirements, and type II diabetes develops. Now that high calorie food is abundantly available and ingested frequently, the prevalence of type II diabetes has skyrocketed.
A number of pathologies develop as type II diabetes advances in severity. Nerves and vasculature become damaged and are the root cause for neuropathy, retinopathy, and nephropathy8. Additionally, cells are unable to uptake glucose necessary for carbon intermediates in central carbon metabolism, leading to ketone body formation and diabetic ketoacidosis10.
Obesity, another metabolic disease, commonly presents alongside type II diabetes. The marked accumulation of excess body fat defining obesity demonstrates the human body’s remarka...


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...ss-talk with endogenous transcription factors which ensures inactive transgene expression in the absence of inducer20. Dimerized EcR and ultraspiracle protein (USP) binds to the ecdysone promoter to recruit RNA polymerase to initiate transcription. The EcR/USP dimer normally exists on the nuclear membrane and only translocates to the nuclear center and binds DNA after intercepting ecdysteroid inducer molecules. The molecular structure of a skeletal ecdysteroid is shown in Figure 1. Numerous ecdysteroids are commercially available and display much variability in binding characteristics to the EcR/USP receptor. For instance, muristerone A binds on the micromolar level and ponasterone A binds at the nanomolar22. Muristerone A might make a better therapeutic inducer because it binds more tightly to EcR/USP than some ecdysteroids, but is lower binding than ponasterone A.

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