Adiposity and β‐Cell Function: Relationships Differ With Ethnicity and Age

The prevalence of type 2 diabetes is higher among African Americans (AA) vs. European Americans (EA), is highest at middle age, and is related to obesity. This study was conducted to test the hypothesis that the association of adiposity (percent body fat (%fat)) with indexes of insulin sensitivity (S_I) and β‐cell function would differ with ethnicity and age. Subjects were 168 healthy, normoglycemic AA and EA girls and women aged 7–12 years, 18–32 years, and 40–70 years. An intravenous glucose tolerance test (IVGTT) was used to assess indexes of insulin secretion and action: S_I, acute C‐peptide secretion (X0); basal, first‐phase, second‐phase, and total β‐cell responsivity to glucose (PhiB, Phi1, Phi2, and Phi_TOT, respectively); and the disposition index (DI = S_I × Phi_TOT). %Fat was assessed with dual energy X‐ray absorptiometrys. Adiposity was significantly associated with S_I among EA (?0.57, P < 0.001) but not AA (?0.20, P = 0.09). Adiposity appeared stimulatory to β‐cell function in the two groups of younger subjects and in EA, but inhibitory in postmenopausal women, particularly AA postmenopausal women. Among AA postmenopausal women, %fat was inversely associated with Phi1 (r = ?0.57, P < 0.05) and Phi_TOT (r = ?0.68, P < 0.01). These results suggest that the impact of adiposity on insulin secretion and action differs with age and ethnicity.     

Adiponectin Levels during Low‐ and High‐Fat Eucaloric Diets in Lean and Obese Women

Objective: Adiponectin influences insulin sensitivity (S_I) and fat oxidation. Little is known about changes in adiponectin with changes in the fat content of eucaloric diets. We hypothesized that dietary fat content may influence adiponectin according to an individual's S_I. Research Methods and Procedures: We measured changes in adiponectin, insulin, glucose, and leptin in response to high‐fat (HF) and low‐fat (LF) eucaloric diets in lean (n = 10) and obese (n = 11) subjects. Obese subjects were further subdivided in relation to a priori S_I. Results: We found significantly higher insulin, glucose, and leptin and lower adiponectin in obese vs. lean subjects during both HF and LF. The mean group values of these measurements, including adiponectin (lean, HF 21.9 ± 9.8; LF, 20.8 ± 6.6; obese, HF 10.0 ± 3.3; LF, 9.5 ± 2.3 ng/mL; mean ± SD), did not significantly change between HF and LF diets. However, within the obese group, the insulin‐sensitive subjects had significantly higher adiponectin during HF than did the insulin‐resistant subjects. Additionally, the change in adiponectin from LF to HF diet correlated positively with the obese subjects’ baseline S_I. Discussion: Although in lean and obese women, group mean values for adiponectin did not change significantly with a change in fat content of a eucaloric diet, a priori measured S_I in obese subjects predicted an increase in adiponectin during the HF diet; this may be a mechanism that preserves S_I in an already obese group.     

β‐Cell Function Improvement After Biliopancreatic Diversion in Subjects With Type 2 Diabetes and Morbid Obesity

In subjects with obesity and type 2 diabetes mellitus (T2DM), biliopancreatic diversion (BPD) improves glucose stimulated insulin secretion, whereas the effects on other secretion mechanisms are still unknown. Our objective was to evaluate the early effects of BPD on nonglucose‐stimulated insulin secretion. In 16 morbid obese subjects (9 with T2DM and 7 with normal fasting glucose (NFG)), we measured insulin secretion after glucose‐dependent arginine stimulation test and after intravenous glucose tolerance test (IVGTT) before and 1 month after BPD. After surgery the mean weight lost was 13% in both groups. The acute insulin response during IVGTT was improved in T2DM after BDP (from 55 ± 10 to 277 ± 91 pmol/l, P = 0.03). A reduction of insulin response to arginine was observed in NFG, whereas opposite was found in T2DM. In particular, acute insulin response to arginine at basal glucose concentrations (AIR_basal) was reduced but insulin response at 14 mmol/l of plasma glucose (AIR₁₄) was increased. Therefore, after BPD any statistical difference in AIR₁₄ between NFG and T2DM disappeared (1,032 ± 123 for NFG and 665 ± 236 pmol/l for T2DM, P = ns). The same was observed for Slope_AIR, a measure of glucose potentiation, reduced in T2DM before BPD but increased after surgery, when no statistically significant difference resulted compared with NFG (Slope_AIR after BPD: 78 ± 11 in NFG and 56 ± 18 pmol/l in T2DM, P = ns). In conclusion, in obese T2DM subjects 1 month after BPD we observed a great improvement of both glucose‐ and nonglucose‐stimulated insulin secretions. The mechanisms by which BDP improve insulin secretion are still unknown.     

β‐Cell Function and Insulin Sensitivity in Adolescents From an OGTT

Given the increase in the incidence of insulin resistance, obesity, and type 2 diabetes in children and adolescents, it would be of paramount importance to assess quantitative indices of insulin secretion and action during a physiological perturbation, such as a meal or an oral glucose‐tolerance test (OGTT). A minimal model method is proposed to measure quantitative indices of insulin secretion and action in adolescents from an oral test. A 7 h, 21‐sample OGTT was performed in 11 adolescents. The C‐peptide minimal model was identified on C‐peptide and glucose data to quantify indices of β‐cell function: static φ_s and dynamic φ_d responsivity to glucose from which total responsivity φ was also measured. The glucose minimal model was identified on glucose and insulin data to estimate insulin sensitivity, S_I, which was compared to a reference measure, S_I^ref, provided by a tracer method. Disposition indices, which adjust insulin secretion for insulin action, were then calculated. Indices of β‐cell function were φ_s = 51.35 ± 8.89 × 10^?9min^?1, φ_d = 1,392 ± 258 × 10^?9, and φ = 82.09 ± 17.70 × 10^?9min^?1. Insulin sensitivity was S_I = 14.19 ± 2.73 × 10^?4, not significantly different from S_I^ref = 14.96 ± 3.04 × 10^?4 dl/kg·min per µU/ml, and well correlated: r = 0.98, P < 0.0001, thus indicating that S_I can be accurately measured from an oral test. Disposition indices were DI_s = 1,040 ± 201 × 10^?14 dl/kg/min² per pmol/l, DI_d = 33,178 ± 10,720 × 10^?14 dl/kg/min per pmol/l, DI = 1,844 ± 522 × 10^?14 dl/kg/min² per pmol/l. Virtually the same minimal model assessment was obtained with a reduced 3 h, 9‐sample protocol. OGTT interpreted with C‐peptide and glucose minimal model has the potential to provide novel insight regarding the regulation of glucose metabolism in adolescents, and to evaluate the effect of obesity and interventions such as diet and exercise.     

Free fatty acid receptor 1 (FFA<Subscript>1</Subscript>R/GPR40) and its involvement in fatty-acid-stimulated insulin secretion

Free fatty acids (FFA) have generally been proposed to regulate pancreatic insulin release by an intracellular mechanism involving inhibition of CPT-1. The recently de-orphanized G-protein coupled receptor, FFA₁R/GPR40, has been shown to be essential for fatty-acid-stimulated insulin release in MIN6 mouse insulinoma cells. The CPT-1 inhibitor, 2-bromo palmitate (2BrP), was investigated for its ability to interact with mouse FFA₁R/GPR40. It was found to inhibit phosphatidyl inositol hydrolysis induced by linoleic acid (LA) (100 μM in all experiments) in HEK293 cells transfected with FFA₁R/GPR40 and in the MIN6 subclone, MIN6c4. 2BrP also inhibited LA-stimulated insulin release from mouse pancreatic islets. Mouse islets were subjected to antisense intervention by treatment with a FFA₁R/GPR40-specific morpholino oligonucleotide for 48 h. Antisense treatment of islets suppressed LA-stimulated insulin release by 50% and by almost 100% when islets were pretreated with LA for 30 min before applying the antisense. Antisense treatment had no effect on tolbutamide-stimulated insulin release. Confocal microscopy using an FFA₁R/GPR40-specific antibody revealed receptor expression largely localized to the plasma membrane of insulin-producing cells. Pretreating the islets with LA for 30 min followed by antisense oligonucleotide treatment for 48 h reduced the FFA₁R/GPR40 immunoreactivity to background levels. The results demonstrate that FFA₁R/GPR40 is inhibited by the CPT-1 inhibitor, 2BrP, and confirm that FFA₁R/GPR40 is indeed necessary, at least in part, for fatty-acid-stimulated insulin release. A. Salehi and E. Flodgren contributed equally to this work     

Racial Differences in Insulin Secretion and Sensitivity in Prepubertal Children: Role of Physical Fitness and Physical Activity

Objective: To investigate in prepubertal children whether physical fitness and/or physical activity are: 1) associated with insulin secretion and sensitivity and 2) account for racial differences in insulin secretion and sensitivity. Research Methods and Procedures: Subjects included 34 African American and 34 white nondiabetic children aged 5 to 11 years. Data were divided into two sets according to the availability of VO_2max and physical activity data. Body composition was measured by dual‐energy X‐ray absorptiometry. Subcutaneous abdominal adipose tissue and intra‐abdominal adipose tissue were examined by computed tomography. Insulin sensitivity (S_I) and acute insulin response (AIR) were determined by a frequently sampled intravenous glucose tolerance test. An all‐out, progressive treadmill exercise test was used for measuring VO_2max. Physical activity data were collected by questionnaire. Results: African American children had lower S_I and higher AIR than white children, after adjusting for total body fat mass. African Americans reported higher levels of physical activity (hours/wk) than whites, but had a lower VO_2max. In multiple linear regression analysis, hours/wk of activity and hours/wk of vigorous activity, but not moderate activity, were independently related to S_I and AIR after adjusting for race, total body fat mass or fat distribution, and total lean tissue mass. VO_2max was not related to AIR, and was inversely related to S_I, after adjusting for body composition. Race remained significantly associated with both S_I and AIR, even after adjusting for body composition, fat distribution, and hours/wk of activity or hours/wk of vigorous activity. Discussion: In summary, overall physical activity and, especially, vigorous activity were associated with insulin secretion and sensitivity. However, neither physical activity nor VO_2max explained the racial difference in insulin secretion (higher in African Americans) and sensitivity (lower in African Americans). Thus, racial (African American to white) differences in aspects of insulin action seem to be due to factors other than body composition, fat distribution, cardiovascular fitness, and amount of physical activity.     

Fat Distribution,Aerobic Fitness,Blood Lipids,and Insulin Sensitivity in African‐American and European‐American Women

The purpose of this study was to determine independent relationships of intra‐abdominal adipose tissue (IAAT), leg fat, and aerobic fitness with blood lipids and insulin sensitivity (S_i) in European‐American (EA) and African‐American (AA) premenopausal women. Ninety‐three EA and ninety‐four AA with BMI between 27 and 30 kg/m² had IAAT by computed tomography, total fat and leg fat by dual‐energy X‐ray absorptiometry, aerobic fitness by a graded exercise test, African admixture (AFADM) by ancestry informative markers, blood lipids by the Ektachem DT system, and S_i by glucose tolerance test. Independent of age, aerobic fitness, AFADM, and leg fat, IAAT was positively related to low‐density lipoprotein–cholesterol (LDL‐C), cholesterol‐high‐density lipoprotein (HDL) ratio, triglycerides (TGs), and fasting insulin (standardized β varying 0.16–0.34) and negatively related to HDL‐cholesterol (HDL‐C) and S_i (standardized β ?0.15 and ?0.25, respectively). In contrast, independent of age, aerobic fitness, AFADM, and IAAT, leg fat was negatively related to total cholesterol, LDL‐C, cholesterol‐HDL ratio, TGs, and fasting insulin (standardized β varying ?0.15 to ?0.21) and positively related to HDL‐C and S_i (standardized β 0.16 and 0.23). Age was not independently related to worsening of any blood lipid but was related to increased S_i (standardized β for S_i 0.25, insulin ?0.31). With the exception of total cholesterol and LDL‐C, aerobic fitness was independently related to worsened blood lipid profile and increased S_i (standardized β varying 0.17 to ?0.21). Maintenance of favorable fat distribution and aerobic fitness may be important strategies for healthy aging, at least in premenopausal EA and AA women.     

Inhibitory effect of obestatin on glucose-induced insulin secretion in rats

Obestatin is a bioactive peptide encoded by the same gene that encodes ghrelin. Our aim was to investigate the effect of obestatin on insulin secretion. We evaluated the effects of obestatin on insulin secretion from rat islet cells which had been incubated overnight in the presence of 8.3, 11.1, and 22.2 mmol/l of glucose. In vivo, the serum levels of glucose and insulin were measured 0, 1, 5, 10, 20, 40, and 60 min after the intravenous administration of saline or glucose (1 g/kg), with or without obestatin, and the area under the 60 min curve of insulin concentration (AUC_insulin) was calculated. Obestatin (0.01-100 nmol/l) inhibited insulin secretion from rat islets in a dose-dependent fashion. In vivo, when administered intravenously to rats together with glucose, obestatin (10, 50, and 250 nmol/kg) inhibited both the rapid 1-min insulin response and the AUC_insulin in a dose-dependent fashion. Our data demonstrate that under glucose-stimulated conditions, exogenous obestatin acts as a potent inhibitor of insulin secretion in anaesthetized rats in vivo as well as in cultured islets in vitro.     

The effect of ACACB cis-variants on gene expression and metabolic traits

Background

Acetyl Coenzyme A carboxylase β (ACACB) is the rate-limiting enzyme in fatty acid oxidation, and continuous fatty acid oxidation in Acacb knock-out mice increases insulin sensitivity. Systematic human studies have not been performed to evaluate whether ACACB variants regulate gene expression and insulin sensitivity in skeletal muscle and adipose tissues. We sought to determine whether ACACB transcribed variants were associated with ACACB gene expression and insulin sensitivity in non-diabetic African American (AA) and European American (EA) adults.

Methods

ACACB transcribed single nucleotide polymorphisms (SNPs) were genotyped in 105 EAs and 46 AAs whose body mass index (BMI), lipid profiles and ACACB gene expression in subcutaneous adipose and skeletal muscle had been measured. Allelic expression imbalance (AEI) was assessed in lymphoblast cell lines from heterozygous subjects in an additional EA sample (n = 95). Selected SNPs were further examined for association with insulin sensitivity in a cohort of 417 EAs and 153 AAs.

Results

ACACB transcribed SNP rs2075260 (A/G) was associated with adipose ACACB messenger RNA expression in EAs and AAs (p = 3.8×10⁻⁵, dominant model in meta-analysis, Stouffer method), with the (A) allele representing lower gene expression in adipose and higher insulin sensitivity in EAs (p = 0.04). In EAs, adipose ACACB expression was negatively associated with age and sex-adjusted BMI (r = −0.35, p = 0.0002).

Conclusions

Common variants within the ACACB locus appear to regulate adipose gene expression in humans. Body fat (represented by BMI) may further regulate adipose ACACB gene expression in the EA population.     

Photosynthesis and photosystem 2 efficiency of two salt-adapted halophytic seashore <Emphasis Type="Italic">Cakile maritima</Emphasis> ecotypes

The effects of salinity (0–400 mM NaCl, marked S₀, S₁₀₀, S₂₀₀, and S₄₀₀) on growth, photosynthesis, photosystem 2 (PS2) efficiency, ion relations, and pigment contents were studied in two seashore Cakile maritima ecotypes (Tabarka and Jerba, respectively, sampled from humid and arid bioclimatic areas). Growth of Jerba plants was improved at S₁₀₀ as compared to S₀. Tabarka growth was inhibited by salinity at all NaCl concentrations. Leaf sodium and chloride concentrations increased with medium salinity and were higher in Jerba than in Tabarka plants. Chlorophyll content, net photosynthetic rate, stomatal conductance (g _s), and intracellular CO₂ concentration were stimulated at moderate salinity (S₁₀₀) in Jerba plants and inhibited at higher salt concentrations in both ecotypes: g _s was the most reduced parameter. The maximum quantum efficiency of PS2 (F_v/F_m), quantum yield, linear electron transport rate, and efficiency of excitation energy capture by open PS2 reaction centres showed no significant changes with increasing salt concentration in Jerba plant and were decreased in Tabarka subjected to S₄₀₀. However, the efficiency of dissipation of excess photon energy in the PS2 antenna was maintained in Jerba and was increased in Tabarka plants challenged with S₄₀₀. Hence the relative salt tolerance of Jerba was associated with a better ability to use Na⁺ and Cl⁻ for osmotic adjustment, the absence of pigment degradation, and the concomitant PS2 protection from photodamage.     

Potential Role of Interleukin‐18 in Liver Disease Associated with Insulin Resistance

Objective: Interleukin (IL)‐18 has been associated with obesity and insulin resistance, both risk factors for the development of liver disease, but the role of IL‐18 in liver disease associated with insulin resistance is presently unknown. We hypothesized that circulating IL‐18 would be related to serum concentrations of liver chemistry tests (LCTs) in apparently healthy subjects and wished to study whether this correlation was dependent on insulin sensitivity (S_I). Research Methods and Procedures: One hundred six apparently healthy white men consecutively enrolled in a cross‐sectional, population‐based study dealing with S_I in men were studied, and S_I (minimal model analysis), LCTs (colorimetry), and IL‐18 serum concentrations (immunoassay) were assessed. Results: Compared with subjects in the lowest quartile for serum IL‐18, subjects in the highest quartile exhibited increased serum triglycerides and decreased S_I, in addition to higher serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (all p < 0.05). The direct association between both ALT and AST and IL‐18 was further confirmed by examining the distribution of serum IL‐18 by quartiles of ALT and AST. Subjects in the highest quartile for serum ALT and AST had higher IL‐18 concentrations compared with subjects in the lowest quartile for these LCTs (both p = 0.01). In multiple regression analysis, IL‐18, but not S_I, was an independent predictor of serum concentrations of ALT and AST, explaining 7% and 4% of their variance, respectively. Discussion: In summary, IL‐18 serum concentrations are associated in apparently healthy humans with plasma concentrations of various LCTs. IL‐18 could contribute to the development of liver disease associated with insulin resistance.     

Fatty acid and very low density lipoprotein metabolism in obese African American and Caucasian women with type 2 diabetes

Type 2 diabetes mellitus (T2DM) is associated with increased plasma triglyceride (TG) concentrations, but African Americans (AA) have lower plasma TG than Caucasians (CC). We evaluated the hypothesis that obese AA women have lower plasma TG than obese CC women do because of differences in lipid kinetics. Eleven AA and 11 CC obese women with T2DM, matched on body mass index (BMI) (AA = 37 ± 1, CC = 37 ± 1 kg/m²), age, duration of diabetes, percentage body fat, and insulin sensitivity (S_I, determined by an intravenous glucose tolerance test), were studied. Plasma TG concentration (AA = 1.14 ± 0.11, CC = 1.88 ± 0.18 mmol/l), FFA rate of appearance (R_a) into plasma (AA = 419 ± 27, CC = 503 ± 31 µmol·min⁻¹), and total VLDL-TG secretion rate (AA = 18 ± 2, CC = 29 ± 4 µmol·min⁻¹) were lower in AA than CC women (all P < 0.05). In contrast, plasma total apolipoprotein (apo)B-100 concentration (AA = 1,542 ± 179, CC = 1,620 ± 118 nmol/l) and VLDL-apoB-100 secretion rate (AA = 1.3 ± 0.1, CC = 1.3 ± 0.1 nmol·min⁻¹) were similar in both groups, so the molar ratio of VLDL-TG secretion rate to VLDL-apoB-100 secretion rate was lower in AA women than in CC women. VLDL-TG concentration was lower in AA women due to lower total VLDL-TG secretion rate. However, the VLDL-apoB-100 secretion rate was the same in both groups, demonstrating that AA women secrete smaller VLDL particles containing less TG than do CC women.     

Relationships between Insulin Sensitivity and Measures of Body Fat in Asymptomatic Men and Women

Objective: To assess whether measures of body fat by DXA scanning can improve prediction of insulin sensitivity (S_I) beyond what is possible with traditional measures, such as BMI, waist circumference, and waist‐to‐hip ratio (WHR). Research Methods and Procedures: Frequently sampled intravenous glucose tolerance tests were performed in 256 asymptomatic non‐Hispanic white subjects from Rochester, MN (age 19‐60 years; 123 men and 133 women) to determine the S_I index by Bergman's minimal model technique. Height, weight, and waist and hip circumferences were measured for calculation of BMI and WHR; DXA was used to determine fat in the head, upper body, abdomen, and lower body. Linear regression was used to assess their relationships with S_I after sex stratification and adjustment for age. Results: After controlling for age, increases in traditional and DXA measures of fat were consistently associated with smaller declines in S_I among women than among men. In men, after controlling for age, all of the predictive information of S_I was provided by waist circumference (additional R² = 0.39, p < 0.001); none of the DXA measures improved the ability to predict S_I. In women, after adjustment for age, BMI, and WHR, the only DXA measure that improved the prediction of S_I was percentage head fat (additional R² = 0.03, p < 0.001). Discussion: Equivalent increases in most measures of body fat had lesser impact on S_I in women than in men. In both sexes, the predictive information provided by DXA measures is approximately equal to, but not additive to, that provided by simpler, traditional measures.     

Adiponectin multimers and metabolic syndrome traits: relative adiponectin resistance in African Americans

African Americans (AAs) tend to have lower total adiponectin levels compared to European Americans (EA); however, it is not known whether race affects adiponectin multimer distribution and their relationships to metabolic traits. We measured total adiponectin, high molecular weight (HMW), low molecular weight (LMW) (i.e., hexamer), and trimer adiponectin in 132 normoglycemic premenopausal women (75 AAs, 57 EAs), together with measures of total and abdominal fat, plasma lipids, insulin sensitivity (S(i)), and genetic admixture estimates. We found that lower total adiponectin in AAs was explained by reduced LMW, and trimer forms because levels of HMW did not differ between races. In EAs, HMW was highly correlated with multiple metabolic syndrome traits. In contrast, the LMW and trimer forms were most highly correlated with metabolic traits in AAs, including abdominal adiposity, lipids, and S(i). At similar levels of visceral adiposity, AAs exhibited significantly lower LMW adiponectin than EAs. Similarly, at comparable levels of HMW and LMW adiponectin, AAs were more insulin resistant than their EA counterparts. In conclusion, (i) serum adiponectin is lower in AAs predominantly as a result of reduced concentrations of LMW and trimers multimeric forms; (ii) LMW and trimer, not HMW, are most broadly correlated with metabolic traits in AAs. Thus, HMW adiponectin may exert less bioactivity in explaining the metabolic syndrome trait cluster in populations of predominant African genetic background.     

Protein Tyrosine Phosphatase 1B Variant Associated with Fat Distribution and Insulin Metabolism

Protein tyrosine phosphatase 1B (PTPN1) affects the regulation of insulin signaling and energy metabolism. We studied whether polymorphisms in the PTPN1 gene impact body fat distribution in the HERITAGE Family Study cohort in 502 white and 276 black subjects. Insulin sensitivity index, glucose disappearance index, acute insulin response to glucose (AIR_glucose), and the disposition index (DI) were obtained from the frequently sampled intravenous glucose tolerance test. White subjects with the G82G at the PTPN1 IVS6+G82A polymorphism had higher body fat levels (p = 0.031) and sum of eight skinfolds (p = 0.003) and highest subcutaneous fat on the limbs (p = 0.002). G82A subjects had the lowest AIR_glucose (p = 0.005) and disposition index (p = 0.040). Interaction effects between PTPN1 and leptin receptor gene variants influenced insulin sensitivity index and AIR_glucose (p from 0.006 to 0.010). The variant PTPN1 Pro387Leu was associated with lower fasting insulin level (p = 0.035) and glucose disappearance index (p = 0.038). In summary, PTPN1 IVS6+G82G homozygotes showed higher levels of all measures of adiposity. G82 allele heterozygotes are potentially at higher risk for type 2 diabetes. Gene‐gene interactions between the PTPN1 and leptin receptor genes contributed to the phenotypic variability of insulin sensitivity. The PTPN1 Pro387Leu variant was associated with lower glucose tolerance.     

Length conversions and mass–length relationships of five forage-fish species in the California current ecosystem

Length-measurement conversions and seasonal mass–length relationships (MLR) for Pacific herring Clupea pallasii, northern anchovy Engraulis mordax, Pacific sardine Sardinops sagax, Pacific mackerel Scomber japonicus and jack mackerel Trachurus symmetricus in the California Current are presented. The conversions between total (L_T), fork (L_F,) and standard lengths (L_S) should facilitate comparisons of data across disciplines and institutions. These equations resulted from an analysis of measurements spanning 14 years and the western seaboard of North America, from the north end of Vancouver Island to the USA–Mexico border. Major-axis regressions were used to calculate reciprocal length-measurement conversions (e.g., L_T to L_S and L_S to L_T) and generalised linear models and ordinary least-squares models were used to create MLRs that account for seasonal variations. The MLR models indicated seasonal differences for all species except C. pallasii, for which there was no multi-season data. Discrepancies between these and published models were examined, along with the suitability and benefit of the various types of models used for length-measurement conversion and MLRs.     

Photosynthesis and the Enzymes of Photosynthetic Carbon Reduction Cycle in Mulberry During Water Stress and Recovery

Net photosynthetic rate (P _N), stomatal conductance (g _S), transpiration rate (E), intercellular CO₂ concentration (C _i), leaf water potential (_w), leaf area, chlorophyll (Chl) content, and the activities of photosynthetic carbon reduction cycle (PCR) enzymes in two mulberry (Morus alba L.) cultivars (drought tolerant Anantha and drought sensitive M-5) were studied during water stress and recovery. During water stress, P _N, g _S, and E declined whereas C _i increased. P _N, g _S, and E were less affected in Anantha than in M-5, which indicates tolerance nature of Anantha over M-5. Activities of ribulose-5-phosphate kinase, NAD- and NADP-glyceraldehyde-3-phosphate dehydrogenases, and 3-phosphoglycerate kinase decreased with increasing stress in both the cultivars. The enzyme activities less affected in tolerant (Anantha) than in sensitive cultivar (M-5) were restored after re-watering to almost initial values in both the cultivars. Re-watering of the plants led to an almost complete recovery of P _N, E, and g _S, indicating that a short-term stress brings about reversible effect in these two cultivars of mulberry.     

Common biological networks underlie genetic risk for alcoholism in African‐ and European‐American populations

Alcohol dependence (AD) is a heritable substance addiction with adverse physical and psychological consequences, representing a major health and economic burden on societies worldwide. Genes thus far implicated via linkage, candidate gene and genome‐wide association studies (GWAS) account for only a small fraction of its overall risk, with effects varying across ethnic groups. Here we investigate the genetic architecture of alcoholism and report on the extent to which common, genome‐wide SNPs collectively account for risk of AD in two US populations, African‐Americans (AAs) and European‐Americans (EAs). Analyzing GWAS data for two independent case–control sample sets, we compute polymarker scores that are significantly associated with alcoholism (P = 1.64 × 10^–3 and 2.08 × 10^–4 for EAs and AAs, respectively), reflecting the small individual effects of thousands of variants derived from patterns of allelic architecture that are population specific. Simulations show that disease models based on rare and uncommon causal variants (MAF < 0.05) best fit the observed distribution of polymarker signals. When scoring bins were annotated for gene location and examined for constituent biological networks, gene enrichment is observed for several cellular processes and functions in both EA and AA populations, transcending their underlying allelic differences. Our results reveal key insights into the complex etiology of AD, raising the possibility of an important role for rare and uncommon variants, and identify polygenic mechanisms that encompass a spectrum of disease liability, with some, such as chloride transporters and glycine metabolism genes, displaying subtle, modifying effects that are likely to escape detection in most GWAS designs.     

Substrate specificity of carboxyl proteinase fromPycnoporus coccineus,a wood-deteriorating fungus

A carboxyl proteinase was purified from submerged-culture filtrate of a wood-deteriorating basidiomycete,Pycnoporus coccineus. The purified enzyme was found to be essentially homogeneous in disc gel electrophoresis tests at pH 9.4 and 2.3. The specificity and mode of action ofP. coccineus carboxyl proteinase I_a were investigated with the oxidized B-chain of insulinP. coccineus carboxyl proteinase I_a hydrolyzed primarily three peptide bonds, Ala¹⁴-Leu¹⁵, Tyr¹⁶-Leu¹⁷, and Phe²⁴-Phe²⁵ bonds, in the oxidized B-chain of insulin.     

Modified minimal model for effect of physical exercise on insulin sensitivity and glucose effectiveness in type 2 diabetes and healthy human

The Bergman’s minimal model of glucose and insulin plasma levels is commonly used to analyse the results of glucose tolerance tests in humans. In this paper, we present the modified minimal model with plasma insulin compartment under the assumption that if the plasma glucose compartment drops below the basal glucose levels, the rate of insulin entering the plasma glucose compartment is zero. Insulin is cleared from the plasma insulin compartment at a rate proportional to the amount of insulin in the plasma insulin compartment. The modified minimal model was used to study the effect of physical exercise via parameters of a mathematical model to qualitative the magnitude of changes in insulin sensitivity (S _I) and glucose effectiveness (S _G) in response to exercise in type 2 diabetes and healthy human. The short-term effects of physical exercise in type 2 diabetes did not improve S _G, but markedly improved the low S _I values found in type 2 diabetes, indicating that the effects of exercise on S _I are quantitatively important in the interpretation of training-related S _I changes and may even be therapeutically useful in type 2 diabetes patients. Physical exercise is indicated either to prevent or delay the onset of type 2 diabetes or to assure a good control of type 2 diabetes by increasing insulin sensitivity.