Summary.Pituitary responsiveness to thyrotrophin releasing hormone (TRH) and luteinizing hormone releasing hormone (LHRH) was studied in thirty one male diabetics, of whom sixteen were insulin-dependent and fifteen on oral ant• agents. Ten age-matched controls were also studied. TRH and LHRH were simultaneously administered intravenously, each in a small dose of 10 ~tg followed two hours later by 190 ~tg and 90 ~tg respectively. Basal hormone levels were measured in a further group of thirty six patients (twelve on insulin, twelve on oral agents and twelve on dietary restrictions alone).Higher thyrotrophin (TSH) response was observed following the small dose of TRH in the patients treated with oral agents than in the control subjects. The response of prolactin was lower in patients treated with oral agents compared with those treated with insulin. There was no difference in plasma 73 and T 4 levels in the patients treated with insulin or oral agents. Significantly higher basal growth hormone (GH) levels were observed in the diabetics. The insulin-dependent group showed a more marked response of GH to TRH/LHRH. No response was observed in the controls. Plasma testosterone levels were significantly lower in the oral agent group (13.8 nmol/1) than in the insulin group (19.4 nmol/1), patients on dietary restrictions (18.4 nmol/1) and the control subjects (19.0 nmol/1). The LH response to the smaller dose of LHRH was impaired in patients on insulin and oral agents. There was a significant difference in FSH response between impotent and sexually normal patients.
SUMMARY
Adrenal tissue, largely composed of the definitive zone, from a newborn anencephalic infant, contained the following enzyme systems: (1) a Δ5-3β-hydroxysteroid dehydrogenase for pregnenolone, demonstrated by the conversion of [14C]pregnenolone to [14C]progesterone; (2) a C(17)-C(20) desmolase, and (3) a steroid 16α-hydroxylase, demonstrated by the conversion of [14C]pregnenolone to [14C]3β, 16α-dihydroxyandrost-5-en-17-one.
The metabolites could not be separated from carrier steroids during sequential partition chromatography. [14C]Progesterone was identified by recrystallization to constant specific activity. [14C]3β, 16α-Dihydroxyandrost-5-en-17-one was identified by enzymatic conversion to [14C]16α-hydroxyoestrone followed by reduction to oestriol and determination of the specific activity of the oestriol after partition chromatography.
It is suggested that these enzymes may play some part in the production of cortisol by the newborn anencephalic infant, and in the provision of precursors for placental oestriol production.
Incubation of [14C] pregnenolone with sliced adrenal tissue from a newborn anencephalic infant yielded [14C] 16α-hydroxy-dehydroepiandrosterone (16α-OH-D). When [3H]dehydroepiandrosterone (D) was incubated with this tissue, [3H] 16α-OH-D could not be detected. Incubation of [3H] pregnenolone and [14C]D together in equimolar quantities yielded 16α-OH-D containing 3H but not 14C. This evidence suggests that 16α-OH-D can be formed in vitro by the adrenal of the newborn anencephalic infant from a C21 steroid by a pathway which avoids D.
16α-OH-D is an efficient precursor of oestriol in late pregnancy. The pathway demonstrated in vitro could therefore provide another source of oestriol precursor from foetal tissues, similar to that which Kirschner et al. (1966) suggested may operate in maternal tissues.
Adrenal tissue from newborn anencephalic infants converted pregnenolone and progesterone to cortisol, 17\g=a\-hydroxyprogesterone,corticosterone, 17\g=a\,21-dihydroxyprogesterone,deoxycorticosterone and 1 1\g=b\-hydroxyprogesterone in vitro. These metabolites were identified by recrystallization to constant specific activity after multiple chromatography and derivative formation. The results demonstrate a potential for corticosteroid biosynthesis, at least from pregnenolone and progesterone, by the adrenals of the anencephalic infant, and therefore possibly by the definitive zone of the adrenal of the normal newborn infant.
Abstract::
Diabetes mellitus (DM) which is defined as high blood glucose level is a major public health worldwide. While discussing DM, the knowledge in this field is unlimited hence a syndrome that populations are living with for more than a decade is always an important matter to keep searching for updates on it. Challenges are always present in different means as comorbidities, poorly controlled DM especially type 2 Diabetes mellitus(T2DM) is considered as a risk factor for a lot of different diseases including but not limited to chronic kidney Disease (CKD). Complications might appear through time, as the aging process changes the body functions, while a significant number of antidiabetic medications are cleared eventually by the kidney; this increase the burden on kidney function placing the diabetic patients at risk. The significant high number of patients with uncontrolled diabetes resulting with kidney disease mirror the importance of this condition on patient’s quality of life. This review presents an overview, pathophysiology, etiology and prevalence of Chronic Kidney Disease (CKD) and abnormal renal parameters correlated with poorly controlled T2DM, with emphasis on and clinical studies involving the association between vitamin D Insufficiency/Deficiency and chronic kidney disease among patients with T2DM.
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