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Blood Glucose, Curcumin, Sugar, And Coffee

October 2017

Blood glucose

Impact of postprandial glucose control on diabetes-related complications: How is the evidence evolving?

Conflicting findings in the literature and lack of long-term definitive outcome studies have led to difficulty in drawing conclusions about the role of postprandial hyperglycemia in diabetes and its complications. Recent scientific publications support the role of postprandial glucose (PPG) as a key contributor to overall glucose control and a predictor of microvascular and macrovascular events. However, the need remains for definitive evidence to support the precise relationship between PPG excursions and the development and progression of cardiovascular complications of diabetes. Drawing firm conclusions on the relationship between PPG and microvascular and macrovascular complications is challenged by the absence of antidiabetic agents that can specifically exert their action on PPG alone, without a basal glucose-lowering effect. Areas under investigation include interventions that more closely approximate 'normal' physiological postprandial responses, as well as technologies that advance the mode of insulin delivery or optimize methods to sense glycemic levels and variation. In conclusion, the precise role of postprandial hyperglycemia in relation to development of diabetic complications is unclarified and is one of the remaining unanswered questions in diabetes. Nevertheless, current evidence supports PPG control as an important strategy to consider in the comprehensive management plan of individuals with diabetes.

J Diabetes Complications. 2016 Mar;30(2):374-85.

Delphinol® standardized maqui berry extract reduces postprandial blood glucose increase in individuals with impaired glucose regulation by novel mechanism of sodium glucose cotransporter inhibition.

AIM: The impetus of our study was to investigate the effects of a nutritional supplement Delphinol®, an extract of maqui berries (Aristotelia chilensis) standardised to ≥25% delphinidins and ≥35% total anthocyanins, on postprandial blood glucose and insulin levels and identify the physiologic mechanism involved. METHODS: Postprandial blood glucose and insulin were investigated in double-blind, placebo-controlled, cross-over fashion in ten volunteers with moderate glucose intolerance. Longer term effects on blood sugar levels were investigated in streptozotocin-diabetic rats over a four months period. Effects of maqui berry delphinidins on sodium-glucose symport were examined in rodent jejenum of the small intestine. RESULTS: Delphinol® intake prior to rice consumption statistical significantly lowered post prandial blood glucose and insulin as compared to placebo. We identified an inhibition of Na+-dependant glucose transport by delphinidin, the principal polyphenol to which Delphinol® is standardised. In a diabetic rat model the daily oral application of Delphinol® over a period of four months significantly lowered fasting blood glucose levels and reached values indistinguishable from healthy non-diabetic rats. CONCLUSION: Our results suggest a potential use of Delphinol® for naturally controlling post-prandial blood glucose owed to inhibition of sodium glucose co-transporter in small intestine.

Panminerva Med. 2014 Jun;56(2 Suppl 3):1-7.

Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men.

Relations between serum lipids, lipoproteins, blood pressure, and insulin metabolism were investigated in 158 healthy men aged 19-77 years and with body mass indexes (BMIs) of 19-41 kg.m-2. Mathematical modeling analysis of glucose, insulin, and C-peptide concentrations during an intravenous glucose tolerance test was used to measure parameters of insulin metabolism. In univariate analysis, both fasting and postglucose insulin concentrations showed significant positive associations with fasting serum triglyceride levels (r = 0.33 and 0.38, respectively) and systolic (r = 0.22 and 0.26) and diastolic (r = 0.21 and 0.24) blood pressure and negative associations with high density lipoprotein subfraction 2 cholesterol (HDL2; r = -0.21 and -0.25). In multivariate analysis, the associations between insulin and HDL2 cholesterol concentrations were found to depend on triglyceride levels. Insulin resistance and basal pancreatic insulin secretion showed significant positive associations with serum triglycerides, which were independent of the effects of age, BMI, and fat distribution. Hepatic insulin throughout was independently associated with HDL2 cholesterol. Associations of insulin-related variables with blood pressure were generally dependent on age and BMI. These results underline the importance of insulin sensitivity and insulin concentrations as determinants of triglyceride metabolism. They also indicate a close relation between hepatic insulin handling and HDL2 concentration that is independent of triglyceride metabolism.

Arterioscler Thromb. 1992 Sep;12(9):1030-5.

Serum Levels of sRAGE Are Associated with Body Measurements, but Not Glycemic Parameters in Patients with Prediabetes.

BACKGROUND: Our aim was to assess serum levels of the soluble receptor for advanced glycation end products (sRAGE) and to examine their association with anthropometric and metabolic parameters in patients with prediabetes and obese controls. METHODS: The two study groups were composed of 42 patients with prediabetes and diabetic neuropathy and 42 age-, gender-, body weight (BW)-, and body mass index (BMI)-matched obese adults as the control group. Prediabetes was diagnosed by the following criteria issued by the American Diabetes Association: impaired fasting glucose [fasting plasma glucose (FPG) level of 100-125 mg/dL], impaired glucose tolerance (2 hr plasma glucose level of 140-199 mg/dL after a 75 grams oral glucose challenge), or a glycated hemoglobin (HbA1C) level of 5.7%-6.4%. RESULTS: There were no differences between the groups in terms of age, gender distribution, BW, or BMI. Despite these similarities, patients with prediabetes had higher FPG, HbA1c, and 2-hr postchallenge glucose levels, higher systolic and diastolic blood pressure, and larger waist and hip circumferences compared with the obese controls. Lipid measurements, complete blood counts, kidney and liver function tests, high-sensitivity C-reactive protein, and sRAGE levels were similar between the two groups. We found significant negative correlations between sRAGE levels and BW, BMI, waist and hip circumferences, waist-to-hip ratios, and low-density lipoprotein (LDL) cholesterol levels. There were no significant correlations with other parameters, including demographic, metabolic, and blood pressure measurements. CONCLUSIONS: In contrast to glycemic parameters, serum levels of sRAGE were negatively correlated with body measurements indicative of obesity in the prediabetic state. In addition, the negative correlation with LDL cholesterol levels suggests that sRAGE has a more robust association with metabolic syndrome than with prediabetes.

Metab Syndr Relat Disord. 2016 Feb;14(1):33-9.

Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men.

Obesity is related to cardiovascular disease (CVD) morbidity and mortality, however, the mechanisms for the development of obesity-induced CVD risk remain unclear. Hyperinsulinemia and insulin resistance are considered key components in the metabolic cardiovascular syndrome and as independent risk factors for CVD. Plasma leptin and tumor necrosis factor-alpha (TNF-alpha), two adipocyte products, are also proposed to be associated with the development of CVD risk. The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. From the Health Professionals Follow-up Study (HPFS), we selected 268 men, aged 47--83 years, who were free of CVD, diabetes, and cancer (except non-melanoma skin cancer), and who had provided a fasting blood sample in 1994. We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m(2)) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. However, plasma leptin may still play a role in CVD through independent effects on lipid metabolism.

Atherosclerosis. 2001 Aug;157(2):495-503.

Hyperinsulinemia is associated with the incidence of hypertension and dyslipidemia in middle-aged men.

Insulin resistance or compensatory hyperinsulinemia has been associated with hypertension and dyslipidemia in cross-sectional studies. In contrast, evidence from prospective population-based studies, which could establish the time order of the relationship, is sparse and inconsistent. Therefore, we investigated the associations of hyperinsulinemia with the incidence of hypertension and dyslipidemia in the Kuopio Ischemic Heart Disease Risk Factor Study, a population-based 4-year follow-up study of middle-aged men from eastern Finland. Out of 975 men who had no diabetes, 543 had resting systolic blood pressure (sBP) of < 165 mmHg and resting diastolic blood pressure (dBP) of < 95 mmHg at baseline and were not taking antihypertensive medication, and 764 had serum triglycerides of < 2.3 mmol/l and HDL cholesterol of > or =1.0 mmol/l at baseline. In logistic regression models adjusted for age, baseline resting blood pressure, baseline lipids, obesity, weight change, and other risk factors, men with hyperinsulinemia (fasting insulin in the highest quintile, > or =12.0 mU/l) at baseline had a 2.0-fold (95% CI 1.1-3.5, P = 0.025) incidence of hypertension (sBP of > or =165 or dBP of > or =95 mmHg), a 2.1-fold (95% CI 1.3-3.4, P = 0.002) incidence of dyslipidemia (serum HDL cholesterol of < 1.0 mmol/l or serum triglycerides of > or =2.3 mmol/l), and a 2.6-fold (95% CI 1.1-6.3, P = 0.028) incidence of the combination of these disorders in 4 years, compared with normoinsulinemic men. These findings demonstrate the role of hyperinsulinemia in incident hypertension and dyslipidemia and suggest that both hypertension and dyslipidemia are associated with insulin metabolism disturbance, independently of obesity and body weight.

Diabetes. 1998 Feb;47(2):270-5.

Mechanisms of insulin resistance in aging.

We have studied 17 elderly and 27 non-elderly, nonobese subjects (mean age 69+/-1 and 37+/-2 yr, respectively) to assess the mechanisms responsible for the abnormal carbohydrate tolerance associated with aging. Serum glucose and insulin levels were significantly elevated in the elderly subjects compared with the nonelderly subjects during a 75-g oral glucose tolerance test, suggesting an insulin resistant state. Peripheral insulin sensitivity was assessed in both groups using the euglycemic glucose clamp technique during an insulin infusion rate of 40 mU/m(2) per min. Similar steady-state serum insulin levels led to a peripheral glucose disposal rate of 151+/-17 mg/m(2) per min in the elderly compared with a value of 247+/-12 mg/m(2) per min in the nonelderly, thus documenting the presence of insulin resistance in the elderly subjects. Insulin binding to isolated adipocytes and monocytes was similar in the elderly and nonelderly groups (2.34+/-0.33 vs. 2.62+/-0.24% and 5.04+/-1.10 vs. 5.12+/-1.07%), respectively. Thus, insulin resistance in the presence of normal insulin binding suggests the presence of a postreceptor defect in insulin action. This was confirmed by performing additional euglycemic clamp studies using infusion rates of 15 and 1,200 mU/m(2) per min to assess the contours of the dose-response relationship. These studies revealed a 39 and 25% decrease in the glucose disposal rate in the elderly subjects, respectively. The results confirm the presence of a postreceptor defect as well as a rightward shift in the dose-response curve. Insulin's ability to suppress hepatic glucose output was less in the elderly subjects during the 15 mU/m(2) per min insulin infusion (77+/-5 vs. 89+/-4% suppression), but hepatic glucose output was fully and equally suppressed in both groups during the 40 and 1,200 mU/m(2) per min infusion. Finally, a significant inverse relationship was observed between the degree of glucose intolerance in the individual elderly subjects, as reflected by the 2-h serum glucose level during the oral glucose tolerance test, and the degree of peripheral insulin resistance as assessed by the glucose disposal rate during the 40 mU/m(2) per min insulin infusion (r = 0.59, P < 0.01).We conclude that carbohydrate intolerance develops as part of the aging process. This carbohydrate intolerance appears to be the consequence of peripheral insulin resistance caused by a postreceptor defect in target tissue insulin action, which causes both a decrease in the maximal rate of peripheral glucose disposal and a rightward shift in the insulin action dose-response curve. In elderly subjects, the severity of the abnormality in carbohydrate tolerance is directly correlated to the degree of peripheral insulin resistance.

J Clin Invest. 1983 Jun;71(6):1523-35.

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