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Purpose Glucose intolerance in pregnancy is likely to occur, as there is an increase in human placenta lactogen by the second trimester. We presumed that changing dietary habits and approximately 10-kg weight gain during pregnancy most likely influenced this condition. Thus, a pregnant woman should be encouraged to reconsider her dietary habits. In this study we examined the factors influencing glucose intolerance with a focus on weight gain and change in dietary habits through the second trimester. Methods This longitudinal study examined pregnant women from the first trimester through the second trimester. We recruited 180 pregnant women who were in their first trimester and who attended a single hospital prenatal clinic between March 2018 and June 2019. Patient characteristics included age, pre-pregnancy body mass index (BMI), maternal weight gain until the second trimester, blood glucose levels in the second trimester, dietary habits, and a brief dietary history questionnaire (BDHQ). A blood glucose level of 140 mg/dl or more during the second trimester placed the patient in the glucose intolerance group and a glucose level less than 140 mg/dl placed the patient in the normal group. Data analysis was performed using the chi-square test and the t-test for the comparison of dietary habits between the first trimester and the second trimester. Binominal logistic regression analysis was used to investigate the factors influencing glucose intolerance. We analyzed the data using the following covariates: pre-pregnancy BMI, weight gain until the second trimester, age, and energy intake. Results A total of 147 pregnant women participated in the study. In the two groups (35 in the glucose group and 112 in the normal group), change in the women's dietary habits included having breakfast, carefully monitoring the speed at which they ate, and checking nutritional facts when they purchased food. Factors influencing glucose intolerance were found to be pre-pregnancy BMI and weight gain until the second trimester. The analysis showed the following results: odds ratio [OR], 1.18; 95% confidence interval [CI], 1.05-1.32, and OR 0.78; 95% CI 0.61-0.99. Conclusion Pregnant women experience nausea, vomiting, and/or changes in their taste for food in the first trimester. However, we considered that nutrition education and an appropriate weight gain until the second trimester would prevent glucose intolerance. In addition, optimal gestational weight gain must be examined in each trimester of gestation. [ABSTRACT FROM AUTHOR]

A 40-year-old female patient was referred to our department with a complaint of postprandial hypoglycemia. We performed a 75g oral glucose tolerance test, and the patient was diagnosed as having impaired glucose tolerance with a 1-hour blood glucose of 245 mg/dl and a 2-hour blood glucose of 196 mg/dl. The patient also showed hypoglycemia with a 6-hour blood glucose of 46 mg/dl, and delayed hypersecretion of insulin, which was diagnosed as reactive hypoglycemia. The patient was diagnosed as having reactive hypoglycemia with delayed hypersecretion of insulin. She was given dietary guidance to avoid simple carbohydrates, and voglibose 0.6 mg was started for glucose intolerance and reactive hypoglycemia. The frequency of hypoglycemic symptoms decreased for a while, but gradually increased again. An interview revealed that the frequency of hypoglycemia was high at 2-3 days before menstruation, and Flash Glucose Monitoring (FGM) was applied to check the blood glucose fluctuation before and after menstruation. Her postprandial hyperglycemia worsened with FGM, and reactive hypoglycemia appeared 3 days before menstruation, while postprandial hyperglycemia improved and reactive hypoglycemia disappeared 4 days after menstruation. The frequency of hypoglycemia was reduced by instructing the patient to take voglibose before menses and to eat a supplementary meal after lunch a few days before menses. There have been no reports on the evaluation of reactive hypoglycemia exacerbated before menstruation by FGM. The menstrual cycle should be considered in the diagnosis, evaluation, and treatment of reactive hypoglycemia.

The prevalence of reflux esophagitis was low in Japan but has increased in recent years. This increase might be due to the increase in the elderly population and obesity with west- ernized diets. Obesity and the metabolic syndrome cause reflux esophagitis. Increase in central obesity induces inflammation in fat tissue. Moreover, insulin resistance induces hypertension, hypertriglyceridemia and impaired glucose tolerance, and causes the metabolic syndrome. Anti-hypertensive drugs (calcium channel blockers, etc.) and hyperglycemia might cause an esophageal movement disorder. Inflammatory state and change of esophageal move- ment might cause and worsen reflux esophagitis. The metabolic syndrome, characterized by central obesity, is a risk factor for reflux esophagitis. It is necessary to consider lifestyle improvements and medications to decrease weight and central obesity.

Preoperative oral hydration is an important component of "enhanced recovery after surgery" strategies. This was originally developed for patients undergoing colon surgery. The Obstetric Anesthesia Practice Guideline issued by American Society of Anesthesiologists states that intake of minimum amount of clear fluid 2 hours prior to surgery may be safe. However, anesthesiologists have to consider physiological changes that parturients undergo during pregnancy, such as increased risk of aspiration and impaired glucose tolerance. We also have to consider the potential effect of glucose loading on neonates. Mothers are more likely to develop ketosis by glucose loading. It also stimulates insulin release in the fetus, which can result in neonatal hypoglycemia. In addition, sodium overloading may deteriorate intra-vascular dehydration and cause lung edema to mothers. On the other hand, oral hydration can alleviate a sense of thirst and increase maternal satisfaction. Our data showed that maternal urinal ketone body at delivery tended to decrease with oral hydration during labor. Moreover, some articles suggest that oral hydration may improve utero-placental perfusion. Therefore, we have to balance risks and benefits of oral hydration in parturients. Further investigations are needed among this specific subgroup of patients in order to establish the safe application of preoperative oral hydration.

In this article, we have reviewed the findings of prospective cohort studies throughout the world to examine influences of lifestyle-related diseases on the risks of total dementia, Alzheimer disease (AD), and vascular dementia (VD). In some cohort studies on elderly populations, diabetes was found to be consistently associated with the risk of VD, but was inconsistently associated with the risk of AD. A cohort study on the elderly residents of the town of Hisayama, Japan, revealed the significant associations between glucose intolerance and the risks of both VD and AD. Clinical and experimental evidence has indicated that glucose intolerance and diabetes induce dementia through various mechanisms such as atherosclerosis,microvascular disease, glucose toxicity, and impaired insulin metabolism. No cohort studies have indicated significant associations between late-life hypertension and the risk of AD, and only 1 study has revealed the significant influence of hypertension on the risk of VD in an elderly population. The Hisayama study revealed that late-life hypertension was a significant risk factor for the development of VD but not for AD. A few cohort studies have suggested the presence of significant associations between midlife hypertension and the risks of late-life AD and VD. Metabolic syndrome has been shown to be a risk factor for the development of cognitive impairment, but no prospective cohort studies have investigated the significant influence of this syndrome on the risk of AD or VD. Some cohort studies have examined the associations of hypercholesterolemia with the risk of AD, but the results were inconsistent. Further studies are required to resolve these issues.

Several studies have shown that fasting blood glucose rises about 1-2 mg/dl/decade and post-prandial glucose by about 15 mg/dl/decade, leading to mild glucose intolerance with insulin resistance associated with aging. There appears to be a distinct group of individuals on an accelerated trajectory to clinically impaired glucose intolerance or frank type 2 diabetes mellitus. There are several characteristics of elderly onset type 2 diabetes as describe below. The incidence and progression of retinopathy were suggested to be rare. Several studies of the association between body mass index and cardiovascular mortality suggested the increased mortality associated with weight loss and underweight. Hypoglycemia is an underappreciated and potentially fatal complication of insulin and sulfonylurea treatment.

Treatment goals of medical care for the elderly patients with diabetes mellitus are maintaining high quality of life and elongating healthy longevity. In order to clarify how the elderly patients with diabetes mellitus should be treated for those purposes, a randomized controlled intervention study using 1,173 Japanese elderly patients with diabetes mellitus is now performing. All subjects have moderate or severe glucose intolerance. Subjects have been divided into two groups, ordinary treatment group and treatment group treated as same as adult patients with diabetes mellitus. The study has not been finished. Therefore, intermediate results were demonstrated and expectation for the study were discussed.

A 73-year-old woman had experienced dry mouth and swellings of both upper eyelids from 1998. In October 2003, she also developed bilateral submandibular swellings, and was diagnosed with diabetes mellitus and prescribed antidiabetic medication. She consulted our hospital in the summer of 2004 due to the exacerbation of eyelid swelling, and was admitted in October 2004. Keratoconjunctivitis sicca was not present. CT and MRI of the head showed bilateral enlargement of the lacrimal and submandibular glands. Serological investigations revealed hypergammaglobulinemia, but as antinuclear antibody and anti-SS-A antibody were absent, further investigation was performed. Serum concentrations of IgG4 were elevated and biopsy of the minor salivary gland revealed a severe infiltration of IgG4-positive plasmacytes. The patient was therefore diagnosed with Mikulicz's disease. Abdominal CT demonstrated diffuse pancreatic swelling, and endoscopic retrograde cholangio-pancreatography revealed stricture of the common bile duct and main pancreatic duct, suggesting the complication of autoimmune pancreatitis. Treatment was commenced with 40 mg/day of prednisolone. This resulted in rapid resolution of the lacrimal and submandibular gland swellings and recovery of salivary gland function. Diffuse swelling of the pancreas and stricture of the common bile duct and main pancreatic duct also improved, and endogenous insulin secretion increased. Both Mikulicz's disease and autoimmune pancreatitis presented with elevated serum IgG4 and infiltration of IgG4-expressing plasma cells into the glandular tissues. We recently proposed the new diagnostic entity of "IgG4-related plasmacytic exocrinopathy"; however, if diabetes mellitus in autoimmune pancreatitis was caused by direct dysfunction of pancreatic cells, we must reconsider this pathogenesis and consider a wider concept including exocrine as well as endocrine glands. This case, in which both types of glands were affected, is therefore of considerable interest.

C-reactive protein (CRP) and serum amyloid A (SAA) are sensitive acute phase reactants. Both, but predominantly CRP in Japan, have long been used for monitoring inflammatory diseases. During the recent wave of measuring both at low concentration ranges and utilizing these values to clarity certain disorders involving low grade inflammation, we need to remain aware of factors other than apparent inflammation that can influence these values. These include age, obesity, hyperlipidemia, glucose intolerance, silent atherosclerosis, and therapeutic use of hypolipidemic agents or glucocorticoid. Genetic polymorphism may also be an influence; especially an allelic variant of SAA1 has been proposed to have a positive effect on SAA concentrations. Understanding this, these values should not be evaluated at a single sampling point but used kinetically in the individual.

Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. These metabolic disturbances have been shown to increase the risk of coronary artery disease. In this theory, insulin resistance and the resultant hyperinsulinemia are considered to raise blood pressure through 1) sympathetic nervous system activation, 2) renal sodium retention, 3) renin-angiotensin system stimulation, and 4) intracellular calcium accumulation in vascular smooth muscle. Indeed, metabolic disturbance and insulin resistance have been pointed out in essential hypertensives. Leptin is a recently discovered hormone produced by an adipocyte-specific ob gene, that contributes to the regulation of energy balance by informing the hypothalamus of the amount of adipose tissue in the body. As a result, the hypothalamus adjusts food intake, thermogenesis, and energy expenditure appropriately. It was clarified that ob gene expression and plasma leptin level in humans were highly correlated with the body mass index, insulin sensitivity and blood pressure. Thus, leptin could play a role in the pathophysiology of insulin-resistant hypertension.

In the last three years, new diagnostic criteria for diabetes mellitus have been proposed by the American Diabetes Association (ADA, 1997), the World Health Organization (WHO) consultation (1998), and the Japan Diabetes Society (JDS, 1999). The most important change from the previous WHO criteria (1985) to these criteria is a decrease in fasting plasma glucose level (FPG) from 140 mg/dl to 126 mg/dl, which defines diabetes mellitus. These criteria attach more importance to FPG than to plasma glucose levels 2 hours after 75 g glucose load (2 hPG). According to these criteria, for example, in one instance with FPG > or = 126 mg/dl, the diagnosis of diabetes mellitus is warranted, if the postprandial plasma glucose > or = 200 mg/dl or another FPG > or = 126 mg/dl were reconfirmed on a subsequent day. The ADA criteria did not recommend an oral glucose tolerance test (OGTT) for routine clinical use. These criteria has established a new category of impaired fasting glucose (IFG) (> or = 110 mg/dl and 126 < mg/dl), similar to impaired glucose tolerance (IGT) which is recognized by performing OGTT. We have reported from a cohort study that there was only one risk factor for IGF: worsening of metabolic derangement progressing to overt diabetes. With IGT, however, there are two risks: a risk for progression to diabetes, and a risk for development of cardiovascular disease. Therefore it seems that whether or not OGTT should be performed depends on the purpose: simply diagnosing for overt diabetes, or detecting risk factors for cardiovascular disease. The JDS criteria proposed the use of HbA1C as a supporting diagnostic tool, because JDS has achieved a fruitful standardization in Japan to a considerable extent. According to the JDS criteria, a diagnosis of diabetes mellitus can be made by an FPG > or = 126 mg/dl when HbA1C > or = 6.5% is confirmed. It is expected that these new criteria will promote further efforts against the increasing number of patients with diabetes mellitus.

Although non-insulin-dependent diabetes mellitus (NIDDM) is essentially a genetic disorder, environmental factors after birth including modernization-westernization and its related life style changes play an important role for the development of diabetes. Former prospective studies have indicated high prevalence of diabetes among the subjects with greater impairement of glucose tolerance, family history of diabetes, history of gestational diabetes and obesity. Beside these, more attention has been paid to the elevation of serum fatty acids and food composition as the provocative factors. In some populations, insulin resistance has been suggested to be a major cause of diabetes. In contrast, we have shown that most of the Japanese patients with NIDDM have impaired early insulin response after glucose loading and this should be important as a predictor for NIDDM.

To determine factors predictive of impaired glucose tolerance (IGT) in the postpartum period, we examined the maternal and perinatal characteristics of fifty-eight women with abnormal glucose tolerance during pregnancy. A 75g oral glucose tolerance test (OGTT) was performed on the women again around 4 weeks after delivery. Forty women who had a 2-hour plasma glucose level of 140mg/dl or more were defined as IGT in postpartum (group IGT), and the other eighteen women with a 2-hour plasma glucose level lower than 140mg/dl were defined as having normalized glucose tolerance (group N). The women in group IGT weighed more during pregnancy than those in group N (p < 0.05). Insulin secretion during the antepartum OGTT was lower in group IGT than in group N. On the basis of the prepregnant body mass index (BMI) for the obese group (BMI > or = 24), the women in group IGT weighed much more during pregnancy than those in group N (p < 0.03). In the non-obese group, the women in group IGT had higher glucose levels and lower insulin responses than those in group N. We concluded that, in obese women, excessive weight gain during pregnancy is predictive of postpartum IGT, while in non-obese women, the severity of glucose intolerance during pregnancy is related to poor postpartum prognosis.