Nonesterified fatty acids

Bihormonal hypothesis" is disturbances of both insulin and glucagon in diabetes mellitus. It resulted in a high blood glucose level. Interestingly, as one of Diabetes Mellitus's risk factors and metabolic disorders, obesity may also play role in altering homeostasis and regulation of glucose metabolism in blood and its utilization in tissues. Unfortunately, there is limited information about the alteration of glucagon levels in various degrees of obesity. This research objective is to learn the plasma glucagon levels alteration in preobese, obese, and very obese persons in Jatinangor in 2015. We had observed 31 obese female subjects in one village. This study was conducted using descriptive quantitative with cross-sectional design. Blood vein samples from the left arm were collected, stored, and transferred to Dr.Hasan Sadikin General Hospital. Glucagon plasma was measured by the ELISA method. We discovered an interesting pattern that showed a correlation between glucose level and the glucagon level in a very obese group. We observed average glucose level is declined and linearly associate with the glucagon level from pre obese to obese and to very obese group. The average level of glucagon in the pre-obese group is 158.62 pg/mL, the obese group is 149.99 pg/mL, and the very obese group is 111.98 pg/ mL. Obesity is one of the factors of metabolic syndrome, which is closely related to various diseases, such as cardiovascular disease and diabetes mellitus type 2. There is a close relationship between obesity and DM type 2. Fifteen thousand six hundred eighty people, ranging from age 35-74, were observed for at least eight years. Interestingly, 28.3% of males with obesity and 31.3% female with obesity then have diabetes mellitus type 2 (Wang et al., 2014). It is due to the adipose tissue in people with obesity can secrete proinflammation factors, which have a great role in the development of insulin resistance (Nehete et al., 2014). In people with diabetes, there are

Prolonged anovulation following parturition has a negative impact on fertility in dairy cows. Insulin plays an important role in ovarian function in many species, and is profoundly depressed in dairy cows during early lactation. We hypothesized that hypoinsulinemia during early lactation represents a key indicator of nutritional status, resulting in delayed ovulation. Holstein cows (n = 10) were subjected to either a hyperinsulinemic–euglycemic clamp (INS) or saline infusion (CTL) for 96 h, beginning on day 10 after parturition during the first postpartum follicular wave. Insulin was infused continuously (0.3 μg/kg body weight per h) via a jugular catheter, and euglycemia was maintained by infusion of glucose. Circulating insulin concentrations were elevated 2.6-fold in INS cows compared with CTL cows (0.73 ± 0.026 vs 0.28 ± 0.026 ng/ml; P < 0.001). Insulin treatment did not affect (P > 0.05) luteinizing hormone (LH) pulse frequency, pulse amplitude or mean circulating LH. Cir...

The nutritionally imbalanced poor-quality diet feeding is the major constraint of dairy production in tropical regions. Hence, alternative high-quality roughage-based diets are required to improve milk yield and reduce methane emission (CH4). Thus, we tested the effects of feeding natural pasture hay, improved forage grass hays (Napier and Brachiaria Hybrid), and treated crop residues (Eragrostis tef straw) on nutrient digestibility, milk yield, nitrogen balance, and methane emission. The eight lactating Fogera cows selected for the experiment were assigned randomly to a 4 × 4 Latin square design. Cows were housed in well-ventilated individual pens and fed a total mixed ration (TMR) comprising 70% roughage and 30% concentrate. The four roughage-based basal dietary treatments supplemented with formulated concentrate were: Control (natural pasture hay (NPH)); treated teff straw silage (TTS); Napier grass hay (NGH); and Brachiaria hybrid grass hay (BhH). Compared with the control diet,...

The innate immune system can immediately respond to microorganism intrusion by helping to prevent further invasion. Bactericidal/permeability-increasing protein (BPI) is a major constituent of neutrophils that possesses anti-inflammatory properties. Inflammation is increasingly recognized as a component of the metabolic syndrome. We hypothesized that the production of BPI could be linked to insulin sensitivity and glucose tolerance. We studied circulating BPI across categories of glucose tolerance. We also studied whether these cross-sectional associations were of functional importance. For this reason, we investigated circulating bioactive lipopolysaccharide and the effects of changing insulin action—after treatment with an insulin sensitizer (metformin)—on circulating BPI in subjects with glucose intolerance. Finally, we tested whether a 3′-untranslated region (UTR) BPI polymorphism led to differences in BPI and insulin action among nondiabetic subjects. Age- and BMI-adjusted circ...

OBJECTIVE-To examine the relationship between fasting plasma insulin and blood pressure (BP) in 40 urbanized normotensive South African black women aged 24-60 yr, and to assess the effects of body mass index (BMI) and fasting plasma glucose on BP. RESEARCH DESIGN ANP METHODS-The women comprised equal numbers of young nonobese nondiaberic subjects, middle-aged nonobese nondiabetic subjects, middle-aged obese nondiabetic subjects, and middle-aged obese newly diagnosed noninsulin-dependent diabetic subjects. Systolic and diastolic BPs were recorded (in duplicate) after 15 min of recumbency, and fasting plasma glucose and insulin levels were determined thereafter. The data were analyzed by simple and multivariate regression. RESULTS-There was a wide distribution of individual physical and biochemical features. With simple correlations, systolic BP correlated significantly with age, BMI, and fasting glucose but not with insulin. Diastolic BP correlated significantly with all four variables (r = 0.37, P < 0.05). When adjusted for age, BMI, and glucose, however, the significant correlation between diastolic BP and insulin diminished (r =-0.04). CONCLUSIONS-As in other nonwhite communities, plasma insulin does not appear to play a major role in regulating the BP of South African black women. T he link between hyperinsulinemia and hypertension is the subject of much controversy (1-3). Reasons for the postulated relationship are unclear but might involve renal sodium retention (4), sympathetic nervous system

It has been postulated that insulin resistance and the concomitant compensatory hyperinsulinemia contribute to the pathogenesis of hypertension, possibly by stimulating the sympathetic nervous system, promoting renal sodium reabsorption, modulating cation transport, and~or stimulating vascular smooth muscle hypertrophy. The purpose of this article is to present a comprehensive up-to-date review of the literature and critically examine the insulin resistance-hyperinsulinemia-hypertension hypothesis.

Diminished insulin (Ins) sensitivity is a characteristic feature of various pathological conditions such as the cardiometabolic syndrome, Type 2 diabetes, and hypertension. Persons with essential hypertension are more prone than normotensive persons to develop diabetes, and this propensity may reflect decreased ability of Ins to promote relaxation and glucose transport in vascular and skeletal muscle tissue, respectively. There are increasing data suggesting that ANG II acting through its ANG type 1 receptor inhibits the actions of Ins in vascular and skeletal muscle tissue, in part, by interfering with Ins signally through phosphatidylinositol 3-kinase (PI3K) and its downstream protein kinase B (Akt) signaling pathways. This inhibitory action of ANG II is mediated, in part, through stimulation of RhoA activity and oxidative stress. Activated RhoA and increased reactive oxygen species inhibition of PI3K/Akt signaling results in decreased endothelial cell production of nitric oxide, ...

Introduction: Insulin resistance always associate pancreatic b -cell dysfunction in type 2 diabetes mellitus.
Obesity is strongly associated with type 2 diabetes mellitus. Therefore screening to evaluate the status of
insulin resistance in offspring of type 2 diabetes mellitus to identify risk of further metabolic complications
is important.
Aims and objectives: The aim of the study is to find out the correlation between insulin resistance in
control with genetic inheritance and obesity.
Materials and Methods: It was a Case control Study carried out on 120 apparently healthy, non-diabetic
people were included in the study. The age of these people lies between 20 to 40 years. The following
anthropometric measurements were done in the above 120 patients. These people were classified depending
upon BMI.
Body Mass Index (BMI) Categorym 18.5–29.99 Non obese 30.0 Obese
Further these people were categorized on the basis of detailed family history of diabetes mellitus to their
parents into 4 different groups and each group contain 30 people as a
a) Group-I (Control): Includes 30 people who were non-obese, off-springs of non-diabetic persons.
b) Group-II (Cases): Includes 30 people who were non-obese, offsprings of type 2 diabetes mellitus
patients.
c) Group-III (Cases): Includes 30 people who were obese, off-springs of non-diabetic persons.
d) Group-IV (Cases): Includes 30 people who were obese, offsprings of type 2 diabetes mellitus.
Conclusion: The purpose of our study was to identify insulin resistance individuals even before appearance
of diabetes mellitus in the above groups by HOM-IR method. So that they can be targeted for aggressive
lifestyle interventions and subsequent morbidity can be prevented.

In assessing the relationship between insulin levels and blood pressure, we analyzed glucose and insulin data after standard 75 g oral glucose tolerance tests in 16 nonobese male Nigerian subjects with essential hypertension and compared their results with those obtained from 16 age- and sex-matched healthy normotensive subjects. The fasting plasma glucose and insulin as well as 2-hour postload insulin values were similar in both groups. The hypertensive subjects had significantly greater 2-hour glucose levels, larger incremental areas under the glucose/time curves, and smaller ratios of incremental insulin to incremental glucose areas (P &lt; .05). These parameters suggest some impairment of glucose tolerance in the hypertensive subjects related to an inadequate insulin response to the oral glucose load. Model analysis of the glucose and insulin data confirmed these observations in that the estimated rate of glucose uptake into peripheral tissues (M value) was lower in the hyperten...

The hypothesis that decreased energy expenditure by the Na,K pump contributes to the development of some forms of obesity remains controversial. Our aim was to study the effects of diet-induced obesity (DIO) on Na,K transport in rat erythrocytes and thymocytes. Sixty six male Sprague Dawley (SD) rats were fed one of three defined diets for nine weeks. The diets were high in saturated fat (HSF; 51% and 12% energy from lard and corn oil, respectively), moderately high in polyunsaturated fat (MPF; 33% energy from corn and safflower oils) or control (C; 12% energy from corn oil) and contained equal amounts of protein (20% energy). Body weights of HSF group were 29% and 23% greater than those of MPF and C groups, respectively. Total body fat as assessed by total body electrical conductivity was 79% and 60% greater in HSF group than in MPF and C groups, respectively;, there were no differences in lean body mass. Metabolic efficiency (nag BWt gained per kJ dietary energy) of HSF groups was 56% and 69% greater than in MPF and C groups. We measured total (nninhibited), ouabain-sensitive (Na,K pump-mediated), bumetanide-sensitive (Na,K, CI cotransportermediated) and ouabain & bumetanide insensitive ('passive') K [8*Rb]influx. In both cell types Na,K pump rates were not lower in the obese HSF group compared to MPF and C groups and thus did not contribute to the increased metabolic efficiency and DIO that were observed. On the contrary, Na,K pump rates were found to be higher (P < 0.05) in thymocytes from the HSF group as compared with results from the MPF group. Because brown adipose tissue is known to be an important site of diet-induced thermogenesis we also studied this tissue. Estimates of BAT thermogenic activity, including uncoupling protein content, indicated a marked stimulation of BAT in the HSF group as compared to the MPF and C groups. It is possible that the dietary stimulation of BAT and of thymic Na,K pump activity are mediated by a common mechanism such as sympathetic stimulation.

To evaluate the relationship between insulin, the renin-aldosterone system and blood pressure in obese subjects. A cross sectional study of a group of severely obese normotensive subjects who were surgical candidates (n=39; mean BMI: 47.8+/-1.4) and a group of hypertensive patients (n=57; mean BMI: 28.0+/-0.7) twenty-nine of whom had BMI&gt;27. All subjects were studied after 15 days on a balanced diet. Insulin, plasma renin activity and aldosterone were measured. Fasting insulin, plasma renin activity and aldosterone were higher in severely obese normotensive subjects than in hypertensive subjects (respectively 32.3+/-3.0 vs 13.1+/-1.0 mU/l, P=0.0001; 1.34+/-0.22 vs 0.88+/-0.12 ng/ml/h, P=0.04; 137.2+/-16.2 vs 87.9+/-12.1 pg/ml, P=0.015). Insulin was related to BMI and to aldosterone both in normotensive and in hypertensive patients. Hyperinsulinemia itself does not determine hypertension; in some people it could play a vasodilator role in opposition to the renin-aldosterone system.

To evaluate the relationship between insulin, the renin-aldosterone system and blood pressure in obese subjects. A cross sectional study of a group of severely obese normotensive subjects who were surgical candidates (n=39; mean BMI: 47.8+/-1.4) and a group of hypertensive patients (n=57; mean BMI: 28.0+/-0.7) twenty-nine of whom had BMI&gt;27. All subjects were studied after 15 days on a balanced diet. Insulin, plasma renin activity and aldosterone were measured. Fasting insulin, plasma renin activity and aldosterone were higher in severely obese normotensive subjects than in hypertensive subjects (respectively 32.3+/-3.0 vs 13.1+/-1.0 mU/l, P=0.0001; 1.34+/-0.22 vs 0.88+/-0.12 ng/ml/h, P=0.04; 137.2+/-16.2 vs 87.9+/-12.1 pg/ml, P=0.015). Insulin was related to BMI and to aldosterone both in normotensive and in hypertensive patients. Hyperinsulinemia itself does not determine hypertension; in some people it could play a vasodilator role in opposition to the renin-aldosterone system.

The innate immune system can immediately respond to microorganism intrusion by helping to prevent further invasion. Bactericidal/permeability-increasing protein (BPI) is a major constituent of neutrophils that possesses anti-inflammatory properties. Inflammation is increasingly recognized as a component of the metabolic syndrome. We hypothesized that the production of BPI could be linked to insulin sensitivity and glucose tolerance. We studied circulating BPI across categories of glucose tolerance. We also studied whether these cross-sectional associations were of functional importance. For this reason, we investigated circulating bioactive lipopolysaccharide and the effects of changing insulin action-after treatment with an insulin sensitizer (metformin)-on circulating BPI in subjects with glucose intolerance. Finally, we tested whether a 3-untranslated region (UTR) BPI polymorphism led to differences in BPI and insulin action among nondiabetic subjects. Age-and BMI-adjusted circulating BPI was significantly lower among patients with type 2 diabetes. Circulating BPI correlated negatively with fasting and postload glucose and insulin concentrations. In subjects with glucose intolerance, BPI was also linked to BMI, waist-to-hip ratio, and age-and BMI-adjusted insulin sensitivity. Bioactive lipopolysaccharide was negatively correlated with circulating BPI (r ‫؍‬ ؊0.57, P < 0.0001) and positively with plasma lipopolysaccharide-binding protein (r ‫؍‬ 0.54, P ‫؍‬ 0.002). In parallel to improved insulin sensitivity, plasma BPI significantly increased in the metformin group but not in the placebo group. A 3-UTR BPI polymorphism was simultaneously associated with plasma BPI concentration, waist-to-hip ratio, fasting and postload insulin concentration, fasting plasma triglycerides, and insulin sensitivity. These findings suggest that this component of the innate immune system is associated with metabolic pathways. . BPI, bactericidal/permeability-increasing protein; CIGMA, continuous infusion of glucose with model assessment; ELISA, enzyme-linked immunosorbent assay; HOMA, homeostasis model assessment; LBP, lipopolysaccharidebinding protein; sTNFR, soluble fraction of tumor necrosis factor-␣ receptor; UTR, untranslated region.

Insulin, glucagon, glucose, nonesterified fatty acids (NEFA), and lactate response to oral glucose tolerance test (OGTT, 75 g glucose) and their correlation with mean blood pressure (BP), were studied in 10 normal subjects (N), 25 subjects with abdominal obesity (O), and 9 subjects with abdominal obesity and IGT or non-insulin-dependent diabetes (OD). O and OD patients, as compared to N subjects, showed increased fasting NEFA, lactate, insulin, and glucagon. NEFA area and insulin total and incremental areas were increased in O and OD (P<0.001 in all instances). Glucagon total area was increased only in OD (P<0.01). Lactate total area was increased in O (P<0.001) and in OD (P<0.01), while lactate incremental area was diminished in O and, even more, in OD subjects (P<0.001 in both instances) and was inversely correlated with the basal level (P<0.001). In all subjects as a whole, increase in NEFA area was weakly correlated with total and incremental insulinemic areas (P<0.05) and more strongly correlated with glucagon and lactate areas (P<0.01). Conversely, the incremental area of lactate was negatively correlated with total insulin (P<0.05), NEFA (P<0.05), and glucagon (P<0.001) areas. BP was increased in O (103.62 ± 2.37) and, even more, in OD (109.41 ± 5.22) compared to N (92.55 ± 0.94 mm Hg), with P<0.01, and was correlated with fasting insulin (P<0.01) and glucose (P<0.05) and, even more, with total (P<0.001) and incremental (P<0.01) insulin areas and NEFA area (P<0.001). Conversely, BP was negatively correlated with incremental lactate area (P<0.01) (similarly to insulin and NEFA area). Our data would suggest that in O and OD patients, insulin resistance is associated with elevated NEFA, insulin and glucagon as well as with high BP. Since NEFA are inhibitors of Na,K-ATPase, they could contribute to elevate BP through the repression of this enzyme (which we have shown previously to be reduced in adipose tissue of obese subjects and correlated negatively with BP).

Insulin Sensitivity Indices for glycemia [ISI(gly)] and blood FFA [ISI(ffa)] can be calculated with the formulas: ISI(gly) = 2/[(INSp x GLYp) + 1], and ISI(ffa) = 2/[(INSp x FFAp) + 1], where INSp, GLYp and FFAp = insulinemic, glycemic, and FFA areas during OGTT (75 g glucose) of the person under study, simplified by considering only data at 0 and 2 h (0-2 h areas), according to WHO criteria or, better, at 0, 1 and 2 h (0-1-2 h areas). Expressed as unit/volume/h, the 0-1-2 h area is equal to 1/2 value at 0 min + value at 1 h + 1/2 value at 2 h, while the 0-2 h area is equal to value at 0 min + value at 2 h. Instead of areas, basal levels can also be used. Basal levels and areas are expressed taking the mean normal value as unit, so that in normal subjects ISI(gly) and ISI(ffa) are always around 1, with maximal variations between 0 and 2. Each laboratory should have its normal reference values for basal levels and OGTT areas. However, reliable mean normal values were selected from literature. Based on meta-analysis of published data, ISI(gly) and ISI(ffa) were reduced in subjects who were overweight and/or IGT and in NIDDM patients and their relatives. Moreover, correlation of ISI(gly) with the euglycemic clamp data was significant. However, it should be stressed that the clamp procedure is performed under artificially induced steady-state whereas ISI(gly) and ISI(ffa) are obtained under rather physiological conditions, with hormonal and metabolic variables unmodified, thus being suitable to assess whole-body insulin sensitivity in the clinical setting.