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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

Octreotide, an analog of somatostatin, is a valid tool for the cure of acromegalic disease. This compound has a prolonged half-life and is more selective than native somatostatin in suppressing growth hormone (GH) secretion. Octreotide, 100 micrograms tid sc, decreases GH levels and improves clinical symptoms in about 85% of acromegalic patients, lowering GH to below 5 ng/ml in 45% and to below 2 ng/ml in 17-21%. Octreotide normalizes somatomedin-C (IGF-I) levels in 36-50% of patients. The increase of dosage up to 1500 micrograms/day does not appear useful in poor responsive patients. No adverse effects on other endocrine functions submitted to hypothalamus-pituitary control have been observed. A slight shrinkage of the pituitary tumor is observed in 30-50% of cases. Octreotide therapy is well tolerated and side effects are usually mild. However the possibility of colelithiasis, liver damage and diabetes mellitus in patients with glucose intolerance must be taken into account. In conclusion octreotide is a useful complement to therapeutic means now used for the treatment of acromegaly.
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PMID:[Treatment of acromegaly with octreotide, a synthetic analog of somatostatin with extended action]. 227 11

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Isolated adrenocorticotropic hormone (ACTH) deficiency was documented after cesarean delivery in a patient with type I diabetes. A preceding severe headache, subsequent declining insulin requirements, and hypotension are consistent with pituitary infarction in a patient without computed tomography evidence of a pituitary tumor. Antepartum incomplete pituitary infarction with isolated ACTH deficiency is an unusual but potentially catastrophic complication of the pregnant diabetic.
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PMID:Isolated adrenocorticotropic hormone deficiency with antepartum pituitary infarction in a type I diabetic. 298 76

We recently reported that insulin inhibits basal and cortisone- and T3-stimulated GH secretion by GH3 rat pituitary tumor cells. The effects of purified semisynthetic human insulin were therefore tested on long-term GH secretion in normal pituitary cells. Primary monolayer cultures derived from male rat pituitaries were grown in serum-free defined medium. Insulin (7 nM) maximally inhibited basal GH secretion by almost 60% after 72 h, with 50% of maximal GH suppression occurring with 1.75 nM insulin. Insulin receptor antiserum blocked the suppression of GH by 7 nM insulin, but had no effect on the suppression of GH by IGF-I (3.25 nM). GRF (100 pM) stimulated GH two- to threefold during 48 h. Insulin (7 nM) prevented the stimulation of GH induced by up to 1 nM GRF (P less than 0.01) and this suppression was also selectively blocked by insulin receptor antiserum. The inhibition of GRF-stimulated GH required a lag period of 48 h and the dose of insulin required for 50% inhibition of GRF stimulation was 3.5 nM. Insulin did not alter the degradation rate of 125I-GH in these cultures and medium glucose concentrations were not different in control or insulin-treated wells for up to 72 h of incubation. The insulin-induced suppression of GH was also observed when cells were grown in glucose-free medium. Insulin did not nonselectively suppress cell secretion, as PRL secretion was mildly stimulated (P less than 0.01) by insulin in the same cultures. Fibroblast growth factor, epidermal growth factor, and insulin A-chain at similar doses did not alter basal or GRF-stimulated GH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1986 Apr
PMID:Effects of insulin on rat anterior pituitary cells. Inhibition of growth hormone secretion and mRNA levels. 308

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.
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PMID:Definition of diabetes mellitus. 351 69

A diabetic cat with hyperadrenocorticism had polydipsia, polyuria, ventral abdominal alopecia, thin dry skin, and a pendulous abdomen. Results of laboratory testing indicated persistent resting hypercortisolemia, hyperresponsiveness of the adrenal glands (increased cortisol concentration) to ACTH gel, and no suppression of cortisol concentrations after administration of dexamethasone at 0.01 or 1.0 mg/kg of body weight. Necropsy revealed a pituitary gland tumor, bilateral adrenal hyperplasia, hepatic neoplasia, and demodicosis. Adrenal gland function was concurrently assessed in 2 cats with diabetes mellitus. One cat had resting hypercortisolemia, and both had hyperresponsiveness to ACTH gel (increased cortisol concentration) at one hour. After administration of dexamethasone (0.01 and 1.0 mg/kg), the diabetic cats appeared to have normal suppression of cortisol concentrations. The effects of mitotane were investigated in 4 clinically normal cats. Adrenocortical suppression of cortisol production occurred in 2 of 4 cats after dosages of 25, 37, and 50 mg/kg. Three cats remained clinically normal throughout the study. One cat experienced vomiting, diarrhea, and anorexia.
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PMID:Hyperadrenocorticism in a cat. 355 96

Insulin has been shown to suppress growth hormone (GH) secretion by rat pituitary tumor cells (GH3) independently of glucose utilization. The effects of physiologic doses of insulin were therefore tested on cytoplasmic levels of GH messenger ribonucleic acid (mRNA) sequences. Insulin (3.5 nM) treatment of cells for 5 days suppressed the hybridization of cytoplasmic GH mRNA with 32P-cDNA for rGH by 50%. The three- to fourfold induction of cytoplasmic GH mRNA by hydrocortisone (1 microM) was also suppressed by insulin (3.5 nM) by 40%. The results show a direct suppression of cytoplasmic rGH mRNA concentration by physiologic doses of insulin. These findings may be due to either decreased rate of GH gene transcription, increased intracellular breakdown, or decreased nuclear-cytoplasmic transport of GH mRNA caused by insulin.
Diabetes 1985 Apr
PMID:Insulin suppresses rat growth hormone messenger ribonucleic acid levels in rat pituitary tumor cells. 388 4

The empty sella results from an extension of the subarachnoid space into an intrasellar position with subsequent remodeling of the sella turcica and the flattening of the pituitary gland. The sella turcica is usually enlarged causing the greatest diagnostic difficulty to distinguish it from a pituitary tumor. The most patients with this syndrome usually have normal pituitary function, while about 30% have varying degrees of hypopituitarism. The Authors describe a case report of a man with primary empty sella syndrome come to the medical observation for obesity and hyperglyccemia. The endocrine evaluation performed (TRH test, GN-RH test, T3, T4, FT3, FT4, Arginine test, metyrapone test) were normal. OGTT shows a maturity onset diabetes (glycemia = 160 mg%). This rare clinical association is not well understood. Probably this diabetes is to the interruption of the normal hypothalamo-pituitary neurovascular connection.
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PMID:[The primary empty sella syndrome. A case report study (author's transl)]. 747 Jan 79

Type I diabetes [insulin-dependent diabetes mellitus (IDDM)] is an autoimmune disease associated with the destruction of pancreatic beta cells. Serum from patients with IDDM increased L-type calcium channel activity of insulin-producing cells and of GH3 cells derived from a pituitary tumor. The subsequent increase in the concentration of free cytoplasmic Ca2+ ([Ca2+]i) was associated with DNA fragmentation typical of programmed cell death or apoptosis. These effects of the serum were prevented by adding a blocker of voltage-activated L-type Ca2+ channels. When the serum was depleted of immunoglobulin M (IgM), it no longer affected [Ca2+]i. An IgM-mediated increase in Ca2+ influx may thus be part of the autoimmune reaction associated with IDDM and contribute to the destruction of beta cells in vivo.
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PMID:Increased activity of L-type Ca2+ channels exposed to serum from patients with type I diabetes. 768 6


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