Explore chapters and articles related to this topic
Lipoprotein lipase deficiency/type I hyperlipoproteinemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Acute attacks are always associated with hyperlipemia. In a patient being successfully managed, they may follow dietary indiscretion or noncompliance. They are especially likely to follow the resumption of a normal diet in an individual who had reduced triglyceride levels by dietary restriction. They may also follow intercurrent infection, and attacks have been related to alcohol. Pregnancy may severely exacerbate symptoms [10] and so may oral contraceptive agents. Many patients learn to regulate their dietary intake of fat in a manner sufficient to eliminate the occurrence of abdominal pains [12].
Type 2 Diabetes in Childhood
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Unfortunately, the long-term success of lifestyle intervention has been disappointing; rates of obesity and IR in children and adults continue to increase despite widespread recognition of the dangers of dietary indiscretion and a sedentary existence. This may reflect in part the resistance of complex feeding and activity behaviors to change, as well as the power of social and economic forces that shape lifestyles in the modern, industrialized world. Metabolic and hormonal adaptations to initial weight loss may also create barriers to long-term success; for example, reductions in food intake and body weight decrease the circulating concentrations of tri-iodothyronine (T3) and leptin and increase circulating concentrations of ghrelin. The fall in T3 and leptin levels limits energy expenditure and sympathetic nervous system activity and may facilitate rebound food intake. Hunger may be intensified by the rise in plasma ghrelin, which stimulates food intake [55]. Food restriction also causes a secondary resistance to growth hormone (GH) action and an increase in insulin sensitivity that may reduce the rates of lipolysis and fat breakdown [56,53]. The obstacles to success with lifestyle intervention have stimulated interest in pharmacologic approaches to diabetes prevention in obese children.
Clinical Features of Colorectal Adenoma and Adenocarcinoma
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Jamie Murphy, Norman S. Williams
In a study by Holiday and Hardcastle,207 99 of 299 patients with colorectal cancer stated that they were ignorant of the implications of their symptoms and 86 did not regard them as serious. Thirty-one believed their symptoms to be due to a dietary indiscretion alone and only 13 (4.3%) mentioned the possibility of cancer. Thirty percent of patients with rectal tumours thought they had piles. Education of the public by doctors and the media might improve this state of affairs. Certainly, such measures for patients with possible breast cancer led to earlier consultation and results from the population-based screening systems demonstrate that screen detected cancers are identified at an earlier stage than non-screen detected tumours. See Chapter 26 in this section.
A pilot dynamic analysis of formative factors of nephrolithiasis related to metabolic syndrome: evidence in a rat model
Published in Renal Failure, 2022
Qiqi He, Yangguo Tang, Yuzhuo Li, Fei Wang, Junsheng Bao, Sanjay Gupta
Animals with MS were more prone to developing hyperoxaluria, which has been widely reported [17,21]. Taguchi K et al. carefully dissected the potential underlying mechanisms of obesity-associated hyperoxaluria in ob/ob mice. However, excluding the contribution of dietary indiscretion, urinary oxalate remained significantly higher in ob/ob mice, suggesting that hyperoxaluria was not solely due to increased oxalate consumption. Hyperoxaluria in MS might be related to systemic inflammation. In particular, an increase in proinflammatory cytokine levels in the intestine could suppress oxalate secretion and contribute to hyperoxaluria [17]. In our study, we found more significant persistent hyperoxaluria in the HFDD group than in the RDD group at each time point. This result indicates that MS promotes the development of hyperoxaluria, which generates inflammation and OS in renal tissue to accelerate crystal formation and deposition.
The leaky lung test: a pilot study using inhaled mannitol to measure airway barrier function in asthma
Published in Journal of Asthma, 2019
Steve Georas, Nicole Ransom, Sara Hillman, Sophia Eliseeva, Janelle Veazey, Timothy Smyth, Kim Le, Jon Meddings
Neither peak mannitol concentrations nor the mannitol AUC correlated with indices of asthma severity including baseline FEV1 or FeNO, or with serum CCSP levels. In fact, mannitol AUC was negatively correlated with both the change in FEV1 after challenge as well as baseline FeNO levels (Figure 5). This suggests that airflow obstruction, airway inflammation, and barrier integrity are regulated by distinct mechanisms, although we acknowledge our small sample size and need for future studies in larger cohorts. We were hoping to use of urinary mannitol clearance as a surrogate of airway barrier function, but wide variability in urine mannitol levels interfered with these analyses. We suspect that dietary indiscretion was one cause of variability (e.g. eating mannitol rich foods), or possibly that some mannitol was swallowed and excreted in stool, but this will need to be followed up in future studies.
Optic neuropathy in classical methylmalonic acidemia
Published in Ophthalmic Genetics, 2019
Mohammed AlOwain, Ola Ali Khalifa, Zahra Al Sahlawi, Maged H Hussein, Raashda A Sulaiman, Moeen Al-Sayed, Zuhair Rahbeeni, Zuhair Al-Hassnan, Hamad Al-Zaidan, Hachemi Nezzar, Iftetah Al Homoud, Abdelmoneim Eldali, Brian Altonen, Bedour S Handoom, Joyce N Mbekeani
Methylmalonic acidemia (MMA) is a relatively common autosomal recessive-inherited metabolic disorder of branched-chain amino acids (isoleucine, valine, methionine and threonine), odd-chained fatty acids and cholesterol. Biochemically, methylmalonic acidemia (MMA, OMIM 609058) is the hallmark of a group of metabolic disorders that disturbs the conversion of methylmalonyl-CoA into succinyl-CoA. The classical form is a consequence of mutation of the MUT gene on chromosome 6, responsible for production of the mitochondrial, methylmalonyl CoA mutase apoenzyme (MCM, EC 5.4.99.2) (1–3). The resultant enzyme deficiency prevents vitamin B12-dependent conversion of methylmalonyl-CoA to succinyl-CoA, required in the Krebs cycle for energy production and the accumulation of methylmalonic acid in various tissues and body fluids. This metabolic disorder is characterized by intermittent periods of potentially lethal metabolic decompensation (metabolic acidosis and/or hyperammonemia), usually triggered by concurrent infection, dietary indiscretion and stress, followed by periods of relatively good clinical health (4,5). These episodes are defined as metabolic crises. Disorders of intracellular cobalamin metabolism caused by impaired synthesis or transport of the cofactor, adenosyl-cobalamin (cblA, cblB and variant 2 of cblD-MMA) exhibit phenotypically similar clinical features to MMA (1,3,4).