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Biomedical subjects

A Garg

Publications and source records attributed to A Garg.

At least 109 records · Page 6Linked to original sources

Relationship of diet, abdominal obesity, and physical activity to plasma lipoprotein levels in Asian Indian physicians residing in the United States.

OBJECTIVE: To examine the relationship of total fat, saturated fat, carbohydrate and energy intake, leisure-time activity, waist-to-hip ratio (WHR), and body mass index to the prevalence of atherogenic plasma triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) levels in Asian Indians living in the United States. High plasma TG and low HDL-C levels have been documented in Asian Indians worldwide. DESIGN: This exploratory study examined medical history, demographics, anthropometrics, plasma lipids levels, food intake frequency, and self-reported leisure-time activity. SUBJECTS: 153 Asian Indian male physicians (mean age=47 years) were recruited at two annual national conferences of the American Association of Physicians from India, with free medical assessments as incentives. STATISTICAL ANALYSES PERFORMED: Correlational and multiple regression analyses were performed. RESULTS: Subjects' diets averaged 56% energy from carbohydrate, 32% from total fat, and 8% from saturated fat. High total fat intake was associated with high WHR (r=.21, P<.01) and high total carbohydrate intake (grams per day) was associated with high TG level (r=.24, P<.05). Leisure-time activity averaged 136 minutes/week and negatively correlated with total plasma cholesterol level (r=.22, P<.01) and low-density lipoprotein cholesterol level (r=.25, P<.001). APPLICATIONS: Dietitians should recommend moderate dietary carbohydrate intake and meal patterns with energy distributed throughout the day, in addition to decreasing fat consumption, to Asian Indian clients at risk for coronary artery disease. High carbohydrate intake and uneven diurnal distribution (no breakfast and large evening meals) are associated with high TG and low HDL-C levels in this population.

Adult↗

RRR-alpha-tocopheryl acetate supplementation at pharmacologic doses decreases low-density-lipoprotein oxidative susceptibility but not protein glycation in patients with diabetes mellitus.

Patients with diabetes mellitus have an increased risk of premature atherosclerosis, which may be due in part to increased oxidizability of low-density lipoprotein (LDL). Numerous studies have shown that alpha-tocopherol can reduce the oxidative susceptibility of LDL in normoglycemic subjects; however, there are few studies in persons with diabetes. In addition, alpha-tocopherol may reduce the extent of protein glycation. Therefore, the objective of the present study was to assess the effect of RRR-alpha-tocopheryl acetate supplementation on LDL oxidizability and protein glycation in persons with diabetes without evidence of vascular disease. Twenty-eight persons with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) were randomly assigned to receive either placebo or 1632 mg (1200 IU) RRR-alpha-tocopherol/d, as tocopheryl acetate, for 8 wk. Plasma and LDL antioxidant concentrations and LDL oxidizability were assessed at both 0 and 8 wk. Plasma and LDL concentrations of alpha-tocopherol were significantly increased in the supplemented group only. Compared with the placebo group, the alpha-tocopherol-supplemented group had significant reductions in LDL oxidizability at 8 wk, as shown by the time-course curves of conjugated diene and lipid peroxide formation. Also, alpha-tocopherol supplementation produced a significant prolongation in the lag phases of both assays, which was evident in both the NIDDM and IDDM subgroups. However, there were no significant changes in glycated hemoglobin or in glycated plasma proteins after alpha-tocopherol supplementation. Thus, alpha-tocopherol supplementation may be beneficial in reducing LDL oxidizability in patients with diabetes.

Adult↗

Relationship of generalized and regional adiposity to insulin sensitivity in men with NIDDM.

Abdominal obesity, particularly excess intraperitoneal fat, is considered to play a major role in causing insulin resistance and NIDDM. To determine if NIDDM patients accumulate excess intraperitoneal fat, and whether this contributes significantly to their insulin resistance, 31 men with mild NIDDM with a wide range of adiposity were compared with 39 nondiabetic, control subjects for insulin sensitivity (measured using euglycemic-hyperinsulinemic clamp technique with [3-3H]glucose turnover) and total and regional adiposity (assessed by hydrodensitometry and by measuring subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses using magnetic resonance imaging [MRI], and truncal and peripheral skinfold thicknesses using calipers). MRI analysis revealed that intraperitoneal fat was not increased in NIDDM patients compared with control subjects; in both groups it averaged 11% of total body fat. NIDDM patients, however, had increased truncal-to-peripheral skinfolds thickness ratios. In NIDDM patients, as in control subjects, amounts of truncal subcutaneous fat showed a stronger correlation with glucose disposal rate than intraperitoneal or retroperitoneal fat; however, NIDDM patients were more insulin resistant at every level of total or regional adiposity. Further, no particular influence of excess intraperitoneal fat on hepatic insulin sensitivity was noted. We conclude that NIDDM patients do not have excess intraperitoneal fat, but that their fat distribution favors more truncal and less peripheral subcutaneous fat. Moreover, for each level of total and regional adiposity, NIDDM patients have a heightened state of insulin resistance.

Adipose Tissue↗

Severe islet amyloidosis in congenital generalized lipodystrophy.

OBJECTIVE: Islet amyloidosis may be one mechanism for pancreatic islet beta-cell loss that is associated with the development of NIDDM. However, the question remains whether chronic overstimulation of insulin and islet amyloid polypeptide (IAPP) secretion in states of insulin resistance could lead to formation of islet amyloidosis and hence NIDDM in some patients. We studied pancreatic islet pathology in congenital generalized lipodystrophy, a genetic syndrome of extreme insulin resistance that may provide some clues. RESEARCH DESIGN AND METHODS: Our patient was a 24-year-old African-American woman with congenital generalized lipodystrophy. Severe acanthosis nigricans was noted in her since age 6. At ages 12 and 16, normal and impaired glucose tolerances, respectively, were noted on oral glucose tolerance tests but were accompanied by extreme fasting and post-prandial hyperinsulnemia. Overt diabetes developed at age 18 and she required approximately 180 U of insulin daily. Immediately after an accidental death at age 24, an autopsy was performed. Pancreatic histology was studied in detail using routine methods and immunohistochemical techniques. RESULTS: Some scarring of the pancreas as a result of previous episodes of acute pancreatitis was observed. Severe amyloidosis was noted in 89% of the islets, sparing those that were rich in pancreatic polypeptide-secreting cells. Amyloid deposits stained intensely on immunostaining with antibodies against amylin. Marked paucity of beta-cells was evident. The ratio of beta- to alpha-cells was reduced to 1:1 (normal ratio approximately 4:1). CONCLUSIONS: These observations suggest that chronic presence of extreme insulin resistance may induce premature and severe islet amyloidosis as well as beta-cell atrophy.

Adult↗

High-fat and high-carbohydrate diets and energy balance.

The current American Diabetes Association guidelines for nutrition recommend a moderate increase in monounsaturated fats and a reduced intake of carbohydrate in patients with diabetes in whom high-carbohydrate diets deteriorate glycemic control and lipoprotein levels. High-fat diets, however, are believed to promote obesity, and some investigators may have reservations recommending such diets. This review thus investigates the role of diet composition in promoting obesity or achieving weight loss and its implications in patients with diabetes. Epidemiological studies show some evidence that fat intake is more importantly related to body weight than carbohydrate intake, but conclusions are weak because confounding variables, such as physical activity, smoking, and energy intake, were generally not controlled for. Metabolic studies under isoenergic conditions report no change in energy balance when fat intake is increased, but report a negative fat balance with substantial increase carbohydrate intake. During overfeeding, excess fat intake is stored as fat, whereas excess carbohydrate is mostly oxidized in the short term but can lead to substantial gain in fat stores because of reduced fat oxidation and considerable de novo lipogenesis in the long term. Spontaneous energy intake, however, is higher on an unrestricted high-fat diet compared with a high-carbohydrate diet, but the long-term effects are not known. Weight-loss intervention studies show that a hypocaloric high-carbohydrate diet is not associated with more weight loss than a high-fat hypocaloric diet. In conclusion, a high-monounsaturated fat diet to control glycemic control and lipoprotein levels in patients with diabetes should not affect weight loss or maintenance, provided that energy intake is carefully controlled.

Cross-Sectional Studies↗

Iduronic acid-rich proteoglycans (PGIdoA) and human post-burn scar maturation: isolation and characterization.

Proteoglycans (PGs) were extracted from human hypertrophic and normal scar tissues from two different stages of maturation after burn injury, under dissociative conditions (4 M guanidinium chloride containing proteinase inhibitors). The extracts were fractionated by ion-exchange chromatography, followed by ethanol precipitation, to give PG-containing iduronic acid (PGIdoA). The size of the PGIdoA decreased with the maturation of scars. Glycosaminoglycan (GAG) chains from PGIdoA were released by alkaline borohydride treatment, and their M(r) values were evaluated by polyacrylamide gel electrophoresis. The M(r) values for PGIdoA protein cores of the hypertrophic scars (5+ years and 2-5 years) and normal scar (5+ years and 2-5 years) were 22.6, 25, 19 and 21 kDa, respectively. The iduronic acid content of PGIdoA from both types of scar increased in their maturation phase. The M(r) values of PGIdoA decreased with maturation. PGIdoA carried the sulfate group mainly attached at C-4 of the 2-amino-2-deoxy-D-galactose residue. The NH2-terminal amino acid sequences of all the PGIdoA were similar to those of normal human skin or bone PG II (decorin) (i.e., Asp-Glu-Ala-B-Gly-Ile-Gly-Pro-Glu-Val-Pro-Asp-Asp-Arg).

Amino Acid Sequence↗

Abnormal cholesterol distribution among lipoprotein fractions in normolipidemic patients with mild NIDDM.

This study was carried out to identify and define lipoprotein abnormalities in patients with noninsulin-dependent diabetes mellitus (NIDDM) who do not have clinical elevations of cholesterol or triglycerides. Thirty-four male patients with mild NIDDM and normolipidemia (plasma cholesterol < or = 240 mg/dl and triglycerides < or = 250 mg/dl) were compared with 35 healthy male normolipidemic subjects. The two groups had similar age and body mass index. Measurements in the two groups included concentrations and chemical composition of lipoproteins and sizing of low-density lipoprotein (LDL) particles. The patients with NIDDM, compared to control subjects, had two distinct lipoprotein abnormalities: first a significantly reduced level of high-density lipoprotein (HDL) cholesterol (mean +/- S.D., 35 +/- 8 mg/dl vs. 41 +/-10 mg/dl, respectively; P = 0.006), and second, a high cholesterol-to-apolipoprotein (apo) B ratio both in a very low density lipoprotein (VLDL) + intermediate density lipoprotein (IDL) fraction (mean +/- S.D.; 3.2 +/- 0.8 vs. 2.8 +/- 0.9, respectively; P = 0.02) and in LDL fraction (mean +/- S.D.; 1.61 +/- 0.11 vs. 1.52 +/- 0.13, respectively; P = 0.003). Increased cholesterol content in LDL was mainly due to free cholesterol. No differences were detected between the two groups in the frequency of LDL pattern A (major LDL peak > 255 A) and pattern B (major LDL peak < or = 255 A). However, a higher frequency of LDL pattern B was found in NIDDM patients with low plasma total triglyceride concentrations ( < 150 mg/dl) compared to the to the control subjects (45% vs. 7%, P = 0.02). Thus in normolipidemic patients with mild NIDDM, the major lipoprotein abnormalities were a low level of HDL cholesterol and compositional changes in LDL and VLDL + IDL fractions. Compositional abnormalities included enrichment of apo B-containing lipoproteins with cholesterol. These lipoprotein abnormalities could have atherogenic potential in patients with mild NIDDM and normolipidemia.

Apolipoproteins B↗

Heterogeneity in adipose tissue metabolism: causes, implications and management of regional adiposity.

The observation that different patterns of adipose tissue distribution are associated with different metabolic abnormalities, has recently given new impetus to research in obesity. Due to several methodologic problems, however, many aspects of regional excess of adipose tissue are still poorly understood. Among them, the causes and the metabolic consequences of regional adiposity are particularly important. Heterogeneity in adipose tissue distribution may be determined by a combination of genetic and hormonal causes. Both factors may determine differences in metabolism of various adipose tissue compartments primarily by regulating LPL production, storage and release of triacylglycerols, and aromatization of androgens. Furthermore, changes in adipocyte sensitivity to hormones such as, sex steroids, glucocorticoids, insulin and adrenergic hormones may also regulate fat distribution in various adipose tissue compartments. The metabolic heterogeneity of adipose tissue from various compartments, particularly the differences between the "portal" and subcutaneous adipose tissues, may account for several metabolic abnormalities associated with "upper body adiposity". However, no direct evidence is available to confirm this hypothesis. Recent advances in the methodology to study adipose tissue distribution (mainly CT and MRI) may provide the necessary tools to evaluate the true impact of adiposity in various compartments on intermediary metabolism and to identify a "morbid" adipose tissue compartment. These observations may help in designing better therapeutic strategies targeted towards regional adiposity and its metabolic complications.

Adipose Tissue↗

Physico-chemical properties of low density lipoproteins in normolipidemic Asian Indian men.

The present study investigated whether a predisposition to high frequency of small, dense low density lipoproteins (LDL) could be an additional coronary risk factor in migrant Asian Indians. Ninety-three normolipidemic (fasting plasma cholesterol levels < or = 240 mg/dl and triglyceride levels < or = 250 mg/dl) adult Asian Indian men residing in the U.S. were compared to a group of 59 Caucasian men for the prevalence of LDL electrophoretic patterns A and B (size of major LDL peak > or = 255 A for LDL pattern A and < 255 A for LDL pattern B). Compared to the Caucasians, the Asian Indians had larger LDL size (mean +/- SD; 260.1 +/- 12.8 A vs 267.7 +/- 11.4 A, respectively; p = 0.0002), an increased frequency of LDL pattern A (59% vs 85%, respectively) and a lower frequency of LDL pattern B (41% vs 15%, respectively) (p = 0.0005). The difference in LDL size in the two study groups persisted after adjusting for the various confounding variables, such as age, plasma triglycerides, high-density lipoprotein cholesterol and dietary habits. We conclude that compared to Caucasians, Asian Indian men have larger LDL particles and a lower prevalence of LDL phenotype B in the presence of normolipidemia. Therefore, we exclude a genetic predisposition to atherogenic LDL phenotype as a factor contributing to the high incidence of coronary heart disease in migrant Asian Indians.

Adult↗

The Strain Index: a proposed method to analyze jobs for risk of distal upper extremity disorders.

Based on existing knowledge and theory of the physiology, biomechanics, and epidemiology of distal upper extremity disorders, a semiquantitative job analysis methodology was developed. The methodology involves the measurement or estimation of six task variables (intensity of exertion, duration of exertion per cycle, efforts per minute, wrist posture, speed of exertion, and duration of task per day); assignment of an ordinal rating for each variable according to exposure data; then assignment of a multiplier value for each variable. The Strain Index is the product of these six multipliers. Preliminary testing suggests that the methodology accurately identifies jobs associated with distal upper extremity disorders versus jobs that are not; however, large-scale studies are needed to validate and update the proposed methodology.

Hand↗

Mechanisms of increase in plasma triacylglycerol concentrations as a result of high carbohydrate intakes in patients with non-insulin-dependent diabetes mellitus.

To determine the mechanisms of increase in plasma triacylglycerol concentrations after high dietary intakes of carbohydrates, 10 men with non-insulin-dependent diabetes mellitus (NIDDM) were fed an isoenergetic high-carbohydrate diet (55% of energy as carbohydrate and 30% as fat) and a high-monounsaturated-fat diet (45% of energy as fat and 40% as carbohydrates) for 6 wk in a randomized, crossover manner. The high-carbohydrate diet raised fasting plasma triacylglycerol concentrations by 26% (P = 0.007) but did not affect postheparin lipoprotein lipase (P = 0.2) or hepatic lipase activities (P = 0.9). The oral-fat-tolerance test labeled with retinyl palmitate also revealed no differences in postprandial plasma triacylglycerol (P = 0.37) or retinyl palmitate clearances (P = 0.34) between the two diets. We conclude that the increase in plasma triacylglycerol concentrations with high-carbohydrate diets in men with NIDDM is not due to reduced lipolysis or diminished postprandial clearance of triacylglycerol-rich lipoproteins but is primarily due to increased hepatic secretion of very-low-density-lipoprotein triacylglycerols.

Aged↗