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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fat cow syndrome developed over a two year period in a 100 cow dairy herd following overfeeding in late lactation and the dry period. It was characterised clinically by a high incidence of parturient paresis and chronic unresponsive ketosis in early lactation. The reproductive performance of the herd was poor throughout this period, with extended calving indices confirming a suggested link between fatty liver and infertility.
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PMID:Fat cow syndrome in a British dairy herd. 664 84

The effect of alcohol on spermatogenesis and morphometric analysis of the human testis was investigated in a prospective autopsy study, with detailed alcohol-use reports from relatives or friends of the deceased. The autopsy series comprised non-alcoholic controls (daily intake < 10 g; n = 32) and heavy-drinkers (n = 44) with an intake of > 80 g per day. Of the controls, 26 (81.3%) men showed normal spermatogenesis, and six (18.7%) partial spermatogenic arrest. Of the heavy drinkers, only 16 (36.4%) had normal spermatogenesis (p < 0.001), while 23 (52.3%) showed partial or complete spermatogenic arrest (p < 0.001) and five had Sertoli cell-only (SCO) syndrome (p < 0.05). The mean testicular weight of heavy-drinkers was slightly (p < 0.05) lower than in the controls. Compared to men with normal spermatogenesis, testicular weight was slightly lower both in controls and heavy-drinkers with spermatogenic arrest, and was significantly (p < 0.01) lower in heavy-drinking men with SCO syndrome. Spermatogenic arrest was not correlated with fatty liver or cirrhosis of the liver, whereas four of the five men with SCO syndrome exhibited a fatty liver. Thus, our results suggest that the most common alcohol-related pathological change in the testes is probably reversible arrest of spermatogenesis. Furthermore, we suggest that many heavy social drinkers may suffer from self-inflicted infertility, as one tenth of heavy-drinkers in our study had SCO syndrome.
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PMID:Spermatogenic arrest and 'Sertoli cell-only' syndrome--common alcohol-induced disorders of the human testis. 774 8

Alanine aminotransferase (ALT) activity was abnormal in 30% of 70 female infertility patients with polycystic ovary syndrome in whom causes other than nonalcoholic fatty liver disease were excluded by history and serum testing. Women with elevated ALT had significantly higher body mass index, waist circumference, serum triglycerides, total cholesterol-to-HDL-cholesterol ratio, and degree of insulin resistance.
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PMID:Abnormal aminotransferase activity in women with polycystic ovary syndrome. 1570 3

We describe a suggestive case of cystic fibrosis (CF) with a CF transmembrane conductance regulator (CFTR) mutation compatible with survival in which the diagnosis was missed in childhood. A 46-year-old man presented to our pediatric hospital with infertility and chronic cough, which had been present since 7 years of age. History was notable for high transaminase levels, hepatic steatosis sinusitis, chronic bronchitis, and duodenal inflammation. A sweat test was performed in duplicate and revealed a near-abnormal chloride level for adult age (77 mEq/L; normal value < 72 mEq/L). Significant findings of chronic bronchitis and bronchiectasis were found on x-ray film. A culture of sputum was positive for Pseudomonas aeruginosa. Spirometry showed a severe airflow limitation (FEV, 40%, and FVC, 61% of the predicted). CFTR mutation analysis showed the presence of homozygous 3849+10kbct mutation. Among CFTR mutations, 3849+ 10kbC>T has been reported frequently in adult patients with normal sweat tests and may cause a late diagnosis of CF. We conclude that because the diagnosis of CF might be missed during childhood, the diagnosis of CF in adults should be considered by practitioners, in subjects with chronic respiratory, gastrointestinal, and hepatic complaints.
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PMID:A missed cystic fibrosis diagnosis in childhood. 1654 75

The cause of low fertility in dairy cows is multifactorial. Poor nutrition during the dry and early postpartum periods results in reduced glucose, insulin, insulin-like growth factor (IGF-I) and low LH pulse frequency with concomitant increases in beta-hydroxy butyrate, non-esterified fatty acids (NEFA) and triacylglycerol. Cows must mobilize large lipid, but also some protein reserves, with a consequent increased incidence of such metabolic disorders as hypocalcaemia, acidosis, ketosis, fatty liver and displaced abomasums. The occurrence of milk fever and ketosis affects uterine contractions, delays calving and increases the risk of retained foetal membranes (RFM) and endometritis. The nutritional risk factors that cause RFM are hypocalcaemia, high body condition score (BCS) at calving and deficiencies in Vitamin E and selenium. The risk factors for endometritis are hypocalcaemia, RFM, high triacylglycerol and NEFA. Thus, metabolic disorders predispose cows to gynaecological disorders, thereby reducing reproductive efficiency. Cows that are overconditioned at calving or those that lose excess body weight are more likely to have a prolonged interval to first oestrus, thereby prolonging days open. Nutritionally induced postpartum anoestrus is characterized by turnover of dominant follicles incapable of producing sufficient oestradiol to induce ovulation due to reduced LH pulse frequency. High nutrition can also increase metabolic clearance rate of steroid hormones such as progesterone or oestradiol. Lower concentrations of oestradiol on the day of oestrus are highly correlated with the occurrence of suboestrus, thereby making the detection of oestrus in high yielding cows even more difficult. Nutrition also affects conception rate (CR) to AI. Cows that develop hypocalcaemia, ketosis, acidosis or displaced abomasums have lower CRs and take longer to become pregnant. Excessive loss of BCS and excess protein content of the ration can reduce CR while supplemental fats that attenuate the production of F2alpha can improve CR. The increased metabolic clearance rate of progesterone (P4), which decreases blood concentrations during early embryo cleavage up to the blastocyst stage is associated with decreased CRs. In conclusion, poor nutritional management of the dairy cow, particularly before and after calving, is a key driver of infertility.
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PMID:The effect of nutritional management of the dairy cow on reproductive efficiency. 1699 5

Polycystic ovary syndrome affects 6%-7% of reproductive-aged women, making it the most common endocrine disorder in this population. It is characterized by chronic anovulation and hyperandrogenism. Affected women may present with reproductive manifestations such as irregular menses or infertility, or cutaneous manifestations, including hirsutism, acne, or male-pattern hair loss. Over the past decade, several serious metabolic complications also have been associated with polycystic ovary syndrome including type 2 diabetes mellitus, metabolic syndrome, sleep apnea, and possibly cardiovascular disease and nonalcoholic fatty liver disease. In addition to treating symptoms by regulating menstrual cycles and improving hyperandrogenism, it is imperative that clinicians recognize and treat metabolic complications. Lifestyle therapies are first-line treatment in women with polycystic ovary syndrome, particularly if they are overweight. Pharmacological therapies are also available and should be tailored on an individual basis. This article reviews the diagnosis, clinical manifestations, metabolic complications, and treatment of the syndrome. A table summarizing treatment recommendations is provided.
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PMID:Polycystic ovary syndrome: diagnosis and treatment. 1727 49

Insulin resistance (IR) in childhood has importance to the understanding and prevention of the growing epidemic of insulin resistance syndrome (IRS) in adults with attendant obesity, type 2 diabetes (T2DM), atherosclerotic diseases, hypertension, gout, non-alcoholic, steato-hepatitis (NASH), gall bladder disease, nephropathy, polycystic ovarian disease (PCOS), infertility and premature senility. The severity of IR and its' complications in children unfortunately and usually progresses in their pubertal transition to adulthood; affected young children are more likely than adults to have underlying causal monogenic disorders; the sequence of natural history and events give insights into disease pathogeneses, and optimal life style choices that last are best made during the early formative years. Some features of IR in children discussed herein are: a strong tendency to low birth weight for gestational age, adverse effects of adrenarche and therapeutic steroid therapy, predisposition to premature pubarche, acanthosis nigricans, tall stature despite pituitary GH suppression, allergic diathesis, hyperandrogenism and PCOS, dyslipidemia and fatty liver disease, and diagnosis by clinical and biochemical markers of IR including insulin regulated hepatic hormonal binding proteins such as IGFBP-1. The national preoccupation with the "metabolic syndrome" T2DM and obesity, should be appropriately directed to an improved understanding of IR in children and their management, if the looming health crisis in affected adults is to be seriously addressed. The nation is facing its' first generation of children who will be less healthy and die younger than the previous generation (Marks (2005) Presentation to the American Association of Diabetes Educators 32nd Annual Meeting and Exhibition, August 10-13, Washington, DC).
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PMID:Childhood obesity and insulin resistance. 1770 76

The severity and frequency of childhood obesity has increased significantly over the past three to four decades. The health effects of increased body mass index as a child may significantly impact obese youth as they age. However, many of the long-term outcomes of childhood obesity have yet to be studied. This article examines the currently available longitudinal data evaluating the effects of childhood obesity on adult outcomes. Consequences of obesity include an increased risk of developing the metabolic syndrome, cardiovascular disease, type 2 diabetes and its associated retinal and renal complications, nonalcoholic fatty liver disease, obstructive sleep apnea, polycystic ovarian syndrome, infertility, asthma, orthopedic complications, psychiatric disease, and increased rates of cancer, among others. These disorders can start as early as childhood, and such early onset increases the likelihood of early morbidity and mortality. Being obese as a child also increases the likelihood of being obese as an adult, and obesity in adulthood also leads to obesity-related complications. This review outlines the evidence for childhood obesity as a predictor of adult obesity and obesity-related disorders, thereby emphasizing the importance of early intervention to prevent the onset of obesity in childhood.
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PMID:Age-related consequences of childhood obesity. 2443 9

Polycystic ovary syndrome (PCOS) affects 5-10% of women of reproductive age, causing a range of reproductive, metabolic and endocrine defects including anovulation, infertility, hyperandrogenism, obesity, hyperinsulinism, and an increased risk of type 2 diabetes and cardiovascular disease. Hyperandrogenism is the most consistent feature of PCOS, but its etiology remains unknown, and ethical and logistic constraints limit definitive experimentation in humans to determine mechanisms involved. In this study, we provide the first comprehensive characterization of reproductive, endocrine, and metabolic PCOS traits in 4 distinct murine models of hyperandrogenism, comprising prenatal dihydrotestosterone (DHT, potent nonaromatizable androgen) treatment during days 16-18 of gestation, or long-term treatment (90 days from 21 days of age) with DHT, dehydroepiandrosterone (DHEA), or letrozole (aromatase inhibitor). Prenatal DHT-treated mature mice exhibited irregular estrous cycles, oligo-ovulation, reduced preantral follicle health, hepatic steatosis, and adipocyte hypertrophy, but lacked overall changes in body-fat composition. Long-term DHT treatment induced polycystic ovaries displaying unhealthy antral follicles (degenerate oocyte and/or > 10% pyknotic granulosa cells), as well as anovulation and acyclicity in mature (16-week-old) females. Long-term DHT also increased body and fat pad weights and induced adipocyte hypertrophy and hypercholesterolemia. Long-term letrozole-treated mice exhibited absent or irregular cycles, oligo-ovulation, polycystic ovaries containing hemorrhagic cysts atypical of PCOS, and displayed no metabolic features of PCOS. Long-term dehydroepiandrosterone treatment produced no PCOS features in mature mice. Our findings reveal that long-term DHT treatment replicated a breadth of ovarian, endocrine, and metabolic features of human PCOS and provides the best mouse model for experimental studies of PCOS pathogenesis.
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PMID:Characterization of reproductive, metabolic, and endocrine features of polycystic ovary syndrome in female hyperandrogenic mouse models. 2487 33

Polycystic ovary syndrome (PCOS) is the most common female endocrinopathy associated with both reproductive and metabolic disorders. Dehydroepiandrosterone (DHEA) is currently used to induce a PCOS mouse model. High-fat diet (HFD) has been shown to cause obesity and infertility in female mice. The possible effect of an HFD on the phenotype of DHEA-induced PCOS mice is unknown. The aim of the present study was to investigate both reproductive and metabolic features of DHEA-induced PCOS mice fed a normal chow or a 60% HFD. Prepubertal C57BL/6 mice (age 25 days) on the normal chow or an HFD were injected (s.c.) daily with the vehicle sesame oil or DHEA for 20 consecutive days. At the end of the experiment, both reproductive and metabolic characteristics were assessed. Our data show that an HFD did not affect the reproductive phenotype of DHEA-treated mice. The treatment of HFD, however, caused significant metabolic alterations in DHEA-treated mice, including obesity, glucose intolerance, dyslipidemia, and pronounced liver steatosis. These findings suggest that HFD induces distinct metabolic features in DHEA-induced PCOS mice. The combined DHEA and HFD treatment may thus serve as a means of studying the mechanisms involved in metabolic derangements of this syndrome, particularly in the high prevalence of hepatic steatosis in women with PCOS.
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PMID:High-fat diet induces significant metabolic disorders in a mouse model of polycystic ovary syndrome. 2510 Jul 14


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