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Biomedical subjects

A Garg

Publications and source records attributed to A Garg.

At least 73 records · Page 4Linked to original sources

Skeletal muscle morphology and exercise response in congenital generalized lipodystrophy.

OBJECTIVE: Congenital generalized lipodystrophy (CGL) is an autosomal recessive genetic disorder characterized by almost complete absence of adipose tissue, muscular appearance, and severe insulin resistance since birth. We investigated whether insulin resistance in CGL patients is associated with abnormal muscle morphology and whether increased muscularity imparts increased muscle strength and exercise capacity RESEARCH DESIGN AND METHODS: We obtained quadriceps muscle biopsies to study muscle fiber types and capillary density in three African-American women (aged 17-20 years) with CGL. We also assessed quadriceps muscle strength, muscle metabolism, and maximal O2 consumption in the patients. RESULTS: Quadriceps muscle biopsies revealed a markedly higher percentage of type II (fast-twitch glycolytic) muscle fibers in patients with CGL versus sedentary young women (75-78 vs. 47-57%, respectively). The capillary-to-fiber ratio (2.7-3.0), however, was normal. Cross-sectional areas of type I (slow-twitch oxidative) (1,262-2,685 microm2) and type II (2,304-3,594 microm2) fibers were far below the normal values (3,811-4,310 and 3,115-4,193 microm2, respectively), suggesting muscle hyperplasia but not hypertrophy The quadriceps muscle strength, as measured by Cybex, was below average; the maximal O2 consumption (23-32 ml x kg(-1) x min(-1)) was also below average. 31P nuclear magnetic resonance spectroscopy of the forearm muscles revealed normal pH and metabolic responses to static and dynamic exercises. CONCLUSIONS: We conclude that insulin resistance in patients with CGL is associated with an increased proportion of type II muscle fibers but not reduced capillary density. Increased muscularity in CGL is due to muscle hyperplasia and is not associated with increased muscle strength.

Adipose Tissue↗

Synovial sarcoma. Large size predicts poor outcome.

A consecutive series of 38 patients with synovial sarcoma diagnosed and treated in a consistent fashion from 1976 to 1994 was reviewed for prognostic variables. The histologic specimens were reviewed and confirmed by one pathologist. There was a minimum 4-year followup for all surviving patients and no patients were lost to followup. The treatment protocol consisted of surgical excision with a wide or radical margin and limb preservation when possible. In those patients in whom the surgical margin was undefined or was less than a wide margin, perioperative radiation therapy was used. Four patients presented with metastatic disease and all died of their disease. Thirty-four patients had localized disease at presentation. Variables considered in stratifying outcomes included histologic grade, histologic subtype, surgical margin, presence or absence of local recurrence, age, and size of tumor. Of the 34 patients without metastasis there was a strong statistical association between size of tumor and survival: 17 patients with tumors less than 5 cm indiameter had a 100% survival, 12 patients with tumors 5 cm to 10 cm had a 75% survival, and five patients with tumors greater than 10 cm had a 20% survival. The authors urge that a multicenter trial for neoadjuvant chemotherapy be initiated for patients presenting with a synovial sarcoma greater than 10 cm in diameter.

Adolescent↗

Right atrial compartmentalization using radiofrequency catheter ablation for management of patients with refractory atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) is often refractory to antiarrhythmic drugs, and patients who are intolerant of AF may require the maze operation for cure. As a less invasive alternative, a catheter-based, right atrial compartmentalization procedure was evaluated. METHODS AND RESULTS: Twelve patients with AF refractory to Class I and III antiarrhythmic drugs were studied. Four linear right atrial radiofrequency ablations were performed, from superior to inferior vena cava in the posterior wall and interatrial septum, anteriorly from the superior vena cava to the tricuspid annulus through the appendage, and across the tricuspid valve-inferior vena cava isthmus. The radiofrequency catheter was dragged along each line three to four times, until the atrial electrogram amplitude decreased by 75% and there was bidirectional conduction block in the tricuspid valve-inferior vena cava isthmus. One complication occurred: sinus node dysfunction requiring a pacemaker. Eight patients were discharged from the hospital on no antiarrhythmic drugs, and four were discharged on previously ineffective antiarrhythmic drugs. Total duration of follow-up was 21.3 +/- 11.2 months. Four patients discharged on previously ineffective antiarrhythmic drugs had no recurrence of AF. One patient discharged off antiarrhythmic drugs had no recurrence of AF. Seven patients discharged off antiarrhythmic drugs had recurrent AF by 12.6 +/- 13.0 months (median 6, range 1 to 39); 3 of these 7 responded to previously ineffective antiarrhythmic drugs without further AF and 4 did not. Thus, 8 of 12 patients (67%) had suppression of AF after ablation on previously ineffective medication or no medication. CONCLUSION: Right atrial compartmentalization may alter the substrate for AF, thus improving the efficacy of previously ineffective antiarrhythmic drugs. Because it is relatively safe, it may be a reasonable adjunctive intervention to maintain sinus rhythm in patients with drug-refractory AF.

Adult↗

Measurement of intracellular triglyceride stores by H spectroscopy: validation in vivo.

We validate the use of 1H magnetic resonance spectroscopy (MRS) to quantitatively differentiate between adipocyte and intracellular triglyceride (TG) stores by monitoring the TG methylene proton signals at 1.6 and 1.4 ppm, respectively. In two animal models of intracellular TG accumulation, intrahepatic and intramyocellular TG accumulation was confirmed histologically. Consistent with the histological changes, the methylene signal intensity at 1.4 ppm increased in both liver and muscle, whereas the signal at 1.6 ppm was unchanged. In response to induced fat accumulation, the TG concentration in liver derived from 1H MRS increased from 0 to 44.9 +/- 13.2 micromol/g, and this was matched by increases measured biochemically (2.1 +/- 1.1 to 46.1 +/- 10.9 micromol/g). Supportive evidence that the methylene signal at 1.6 ppm in muscle is derived from investing interfascial adipose tissue was the finding that, in four subjects with generalized lipodystrophy, a disease characterized by absence of interfacial fat, no signal was detected at 1.6 ppm; however, a strong signal was seen at 1.4 ppm. An identical methylene chemical shift at 1.4 ppm was obtained in human subjects with fatty liver where the fat is located exclusively within hepatocytes. In experimental animals, there was a close correlation between hepatic TG content measured in vivo by 1H MRS and chemically by liver biopsy [R = 0.934; P <.0001; slope 0.98, confidence interval (CI) 0.70-1.17; y-intercept 0.26, CI -0.28 to 0. 70]. When applied to human calf muscle, the coefficient of variation of the technique in measuring intramyocellular TG content was 11.8% in nonobese subjects and 7.9% in obese subjects and of extramyocellular (adipocyte) fat was 22.6 and 52.5%, respectively. This study demonstrates for the first time that noninvasive in vivo 1H MRS measurement of intracellular TG, including that within myocytes, is feasible at 1.5-T field strengths and is comparable in accuracy to biochemical measurement. In addition, in mixed tissue such as muscle, the method is clearly advantageous in differentiating between TG from contaminating adipose tissue compared with intramyocellular lipids.

Adipose Tissue↗

Adipose tissue distribution pattern in patients with familial partial lipodystrophy (Dunnigan variety).

Familial partial lipodystrophy, Dunnigan type (FPLD), is a rare autosomal dominant genetic disorder characterized by gradual loss of sc fat from the extremities, commencing at the time of puberty. Excess fat deposition may occur in the face and neck area. Limited information is available about adipose tissue distribution in patients with FPLD. To investigate whether there is a unique pattern of fat distribution in both affected men and women with FPLD, we performed whole-body magnetic resonance imaging in one male and three female patients from two pedigrees. Magnetic resonance imaging studies confirmed the clinical findings of near-total absence of sc fat from all extremities. Reduction in sc adipose tissue from the truncal area was more prominent anteriorly than posteriorly. Increased fat stores were observed in the neck and face. Intermuscular adipose tissue in the extremities and pelvic area were subjectively increased. Intraabdominal and intrathoracic adipose tissue was not reduced. Bone marrow fat, as well as mechanical adipose tissue, was present in normal amounts. The pattern of fat distribution in the male and females was similar. We conclude that FPLD results in a characteristic absence of sc fat from the extremities, with preservation of intermuscular fat stores.

Adipose Tissue↗

Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men.

It has been proposed that excessive insulin resistance in Asian Indians living in urban areas or migrated to western countries is responsible for the higher incidence of type 2 diabetes and coronary heart disease observed in this population. To evaluate whether Asian Indians are more insulin resistant than Caucasians and to define the role of generalized and truncal adiposity, we performed hydrodensitometry, skinfold measurements, and euglycemic-hyperinsulinemic clamps in 21 healthy Asian Indian men and 23 Caucasian men of similar age and body fat content. The glucose disposal rate (Rd) was significantly lower in the Asian Indians than in the Caucasians (3.7+/-1.3 vs. 5.3+/-2.0 mg/min x kg lean body mass, respectively; P = 0.003). Despite similar total body fat content, Asian Indians had higher truncal adiposity than Caucasians (sum of truncal skinfolds, 117+/-37 and 92.4+/-38 mm, respectively). In both Asian Indians and Caucasians, the insulin sensitivity index (Rd/plasma insulin concentrations) was inversely correlated with both total body fat (r = -0.49; P<0.03 and r = -0.67; P<0.001, respectively) and sum of truncal skinfold thickness (r = -0.55; P<0.001 and r = -0.61; P<0.002, respectively). After adjustment for total body fat and truncal skinfold thickness, Asian Indians still had a significantly lower glucose disposal rate (P = 0.04). These results show that Asian Indian men are more insulin resistant than Caucasian men independently of generalized or truncal adiposity. The excessive insulin resistance in Asian Indians is probably a primary metabolic defect and may account for the excessive morbidity and mortality from diabetes and coronary heart disease in this population.

Adult↗

A gene for congenital generalized lipodystrophy maps to human chromosome 9q34.

Congenital generalized lipodystrophy (CGL, Berardinelli-Seip Syndrome, OMIM # 269700) is a rare autosomal recessive disorder characterized by near complete absence of adipose tissue from birth. Affected individuals have marked insulin resistance, hypertriglyceridemia and acanthosis nigricans, and develop diabetes mellitus during teenage years. The genetic defect for CGL is unknown. A semi-automated genome-wide scan with a set of highly polymorphic short tandem repeats (STR) was carried out in 17 well-characterized pedigrees and identified a locus for CGL to chromosome 9q34. The maximum two-point lod score obtained was 3.6 at D9S1818 (theta(max) = 0.05). There was evidence for genetic heterogeneity (alpha = 0.73) and 2 of the pedigrees were unlinked. Multipoint linkage analysis excluding the 2 unlinked families yielded a peak lod score of 5.4 between loci D9S1818 and D9S1826. The CGL1 critical region harbors a plausible candidate gene encoding the retinoid X receptor alpha (RXRA) that plays a central role in adipocyte differentiation. Identification of the CGL gene(s) will contribute to our understanding of the adipocyte differentiation and elucidation of the mechanisms of insulin resistance in disorders of adipose tissue.

Acanthosis Nigricans↗

Acute and chronic stress-induced oxidative gastrointestinal mucosal injury in rats and protection by bismuth subsalicylate.

Reactive oxygen species (ROS) are implicated in the pathogenesis of stress-induced gastrointestinal mucosal injury. In the present study, we have investigated the effects of acute and chronic stress on the enhanced production of ROS including superoxide anion [SA; as determined by cytochrome c reduction (CCR)] and hydroxyl radicals (OH), and correlated the enhanced production of these free radicals with increased lipid peroxidation, membrane microviscosity and DNA fragmentation, indices of oxidative tissue damage, in the gastric and intestinal mucosa of female Sprague-Dawley rats. Furthermore, the protective ability of bismuth subsalicylate (BSS) against the gastrointestinal mucosal injury induced by acute and chronic stress was determined. Acute stress was induced for a period of 90 min, while chronic stress was induced for 15 min/day for 15 consecutive days. Half of the animals exposed to acute stress were pretreated orally with 15 mg BSS/kg 30 min prior to the exposure to acute stress. Similarly, half of the animals exposed to water-immersion restraint chronic stress were pretreated orally with 7.5 mg BSS/kg/day for 15 consecutive days 30 min prior to the exposure to chronic stress. Acute stress produced greater injury to both gastric and intestinal mucosa as compared to chronic stress. Acute stress increased CCR and OH production by 10.0- and 14.3-fold, respectively, in the gastric mucosa, and 10.4- and 17.0-fold, respectively, in the intestinal mucosa. Pretreatment with BSS prevented the acute stress-induced increase in CCR and OH production. Acute stress increased lipid peroxidation, DNA fragmentation and membrane microviscosity by 3.6-, 4.0- and 11.6-fold, respectively, in gastric mucosa, and 4.1-, 5.0- and 16.2-fold, respectively, in intestinal mucosa. BSS decreased acute stress-induced lipid peroxidation, DNA fragmentation and membrane microviscosity by approximately 26, 35 and 30%, respectively, in gastric mucosa, and by 20, 36 and 30%, respectively, in the intestinal mucosa. Chronic stress increased CCR and OH production by 4.8- and 6.3-fold, respectively, in gastric mucosa, and 4.6- and 6.9-fold, respectively, in intestinal mucosa. Chronic stress increased lipid peroxidation and DNA fragmentation by 2.9- and 3.3-fold, respectively, in gastric mucosa, and 3.3- and 4.2-fold, respectively, in intestinal mucosa. BSS decreased chronic stress-induced lipid peroxidation, DNA fragmentation and membrane microviscosity by approximately 41, 44 and 45%, respectively, in gastric mucosa, and by 39, 52 and 51%, respectively, in the intestinal mucosa. Daily administration of BSS provided greater protection against chronic stress-induced oxidative gastrointestinal injury as compared to the acute stress. These results demonstrate that both acute and chronic stress can induce gastrointestinal mucosal injury through enhanced production of ROS, and that BSS can significantly protect against gastrointestinal mucosal injury.

Animals↗

Monogenic disorders of obesity and body fat distribution.

Recently, great progress has been made towards understanding the molecular basis of body fat regulation. Identification of mutations in several genes in spontaneous monogenic animal models of obesity and development of transgenic models have indicated the physiological roles of many genes in the regulation of body fat distribution. In humans, mutations in leptin, leptin receptor, prohormone convertase 1 (PC1), pro-opiomelanocortin (POMC), melanocortin 4-receptor (MC4-R), and peroxisome proliferator-activated receptor (PPAR) gamma2 genes have been described in patients with severe obesity. Most of these obesity disorders exhibit a distinct phenotype with varying degrees of hypothalamic and pituitary dysfunction and a recessive inheritance, whereas MC4-R mutation has a nonsyndromic phenotype with dominant inheritance. These mutations suggest the critical role of central signaling systems composed of leptin/leptin receptor and alpha-melanocyte stimulating hormone/MC4-R in human energy homeostasis. Although the genetic basis of monogenic disorders of body fat distribution, such as congenital generalized lipodystrophy and familial partial lipodystrophy, Dunnigan variety, is still unknown, the genes for these have recently been localized to chromosomes 9q34 and 1q21-22, respectively. The advances in our knowledge of the phenotypic manifestations and underlying molecular mechanisms of genetic body fat disorders may lead to better treatment and prevention of obesity and other disorders of adipose tissue in the future.

Adipose Tissue↗

The ineffectiveness of immunosuppressive therapy in lymphocytic myocarditis: an overview.

BACKGROUND: The use of immunosuppressive therapy for myocarditis is controversial. PURPOSE: To review the literature on the effectiveness of immunosuppressive therapy in biopsy-proven lymphocytic myocarditis. DATA SOURCES: Two authors independently searched MEDLINE and other medical databases from 1980 to 26 June 1997. STUDY SELECTION: Randomized, controlled trials; matched-cohort studies; and case-control studies of patients with biopsy-proven myocarditis (Dallas criteria or a mean of > or = 2.5 lymphocytes per high-power field) for which any form of immunosuppressive treatment was used. The outcomes of interest were mortality and change in left ventricular ejection fraction. DATA EXTRACTION: 6 of 374 studies satisfied the selection criteria. DATA SYNTHESIS: In survivors, left ventricular function in myocarditis improved approximately 10% over 6 months without immunosuppressive treatment. Prednisone alone did not improve survival (P >0.2) or left ventricular function (P >0.11). Prednisone combined with azathioprine or cyclosporine did not improve survival (P >0.2) or left ventricular function (P >0.2) in three studies. However, one small matched-cohort study showed improvement in children (P <0.01). Neither interferon nor thymic hormone improved survival or left ventricular function. CONCLUSIONS: Immunosuppressive therapy is ineffective in lymphocytic myocarditis. Current therapy in lymphocytic myocarditis seems to be limited to supportive measures or transplantation.

Clinical Trials as Topic↗

Treatment of diabetic dyslipidemia.

Patients with diabetes mellitus have an increased risk for coronary artery disease due to hyperglycemia, hypertension, dyslipidemia, and other risk factors. The diabetic dyslipidemia in these patients is characterized by moderately high levels of (1) serum cholesterol and triglycerides; (2) small, dense low-density lipoprotein (LDL) particles; and (3) low high-density lipoprotein (HDL) cho-lesterol concentrations. Recent clinical trials have demonstrated the benefits of cholesterol-lowering therapy in both diabetic and nondiabetic patients, thus supporting aggressive treatment of diabetic dyslipidemia for coronary artery disease prevention. A 3-step approach is recommended for the treatment of diabetic dyslipidemia. First, modification of diet and lifestyle, including decreased intakes of cholesterol, cholesterol-raising fats, and total energy, and increased physical activity should be advised. Second, good glycemic control should be achieved with diet and hypoglycemic drugs, if needed. Third, lipid-lowering drugs should be used, if necessary. Non-HDL cholesterol levels, which include both very-low-density lipoprotein (VLDL) and LDL cholesterol, should be the target of cholesterol-lowering therapy. The use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (the "statins") has become the first-line drug therapy for diabetic dyslipidemia. Bile acid sequestrants are effective cholesterol-lowering agents in normotriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients with severe hypertriglyceridemia may require fibric acids or n-3 polyunsaturated fatty acids. Nicotinic acid worsens hyperglycemia; therefore, it should be avoided in most cases. The efficacy and safety of estrogen-replacement therapy in postmenopausal women with diabetes needs to be determined. The combination of two lipid-lowering agents may be appropriate for some NIDDM patients but should be used judiciously.

Cholesterol, Dietary↗

Sibling rivalry and the gender gap: evidence from child health outcomes in Ghana.

"When capital and labor markets are imperfect, choice sets narrow, and parents must choose how to ration available funds and time between their children. One consequence is that children become rivals for household resources. In economies with pro-male bias, such rivalries can yield gains to having relatively more sisters than brothers. Using a rich household survey from Ghana [the 1988-1989 Ghana Living Standards Survey], we find that on average if children had all sisters (and no brothers) they would do roughly 25-40% better on measured health indicators than if they had all brothers (and no sisters)."

Africa↗

Protective effects of grape seed proanthocyanidins and selected antioxidants against TPA-induced hepatic and brain lipid peroxidation and DNA fragmentation, and peritoneal macrophage activation in mice.

1. The comparative protective abilities of a grape seed proanthocyanidin extract (GSPE) (25-100 mg/kg), vitamin C (100 mg/kg), vitamin E succinate (VES) (100 mg/kg) and beta-carotene (50 mg/kg) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced lipid peroxidation and DNA fragmentation in the hepatic and brain tissues, as well as production of reactive oxygen species by peritoneal macrophages, were assessed. 2. Treatment of mice with GSPE (100 mg/kg), vitamin C, VES and beta-carotene decreased TPA-induced production of reactive oxygen species, as evidenced by decreases in the chemiluminescence response in peritoneal macrophages by approximately 70%, 18%, 47% and 16%, respectively, and cytochrome c reduction by approximately 65%, 15%, 37% and 19%, respectively, compared with controls. 3. GSPE, vitamin C, VES and beta-carotene decreased TPA-induced DNA fragmentation by approximately 47%, 10%, 30% and 11%, respectively, in the hepatic tissues, and 50%, 14%, 31% and 11%, respectively, in the brain tissues, at the doses that were used. Similar results were observed with respect to lipid peroxidation in hepatic mitochondria and microsomes and in brain homogenates. 4. GSPE exhibited a dose-dependent inhibition of TPA-induced lipid peroxidation and DNA fragmentation in liver and brain, as well as a dose-dependent inhibition of TPA-induced reactive oxygen species production in peritoneal macrophages. 5. GSPE and other antioxidants provided significant protection against TPA-induced oxidative damage, with GSPE providing better protection than did other antioxidants at the doses that were employed.

Animals↗

Dyslipoproteinemia and diabetes.

Dyslipidemia in patients with diabetes constitutes quantitative and qualitative abnormalities in all classes of lipoproteins and may be a significant contributor to the high risk of atherosclerosis in these patients. A step-care approach to therapy of diabetic dyslipidemia, including hygienic measures (diet and increased physical activity), hypoglycemic drugs, and lipid-lowering drugs, is recommended. The choice of lipid-lowering drugs depends on severity of hypertriglyceridemia. Statins and bile-acid-binding resins are the choice of therapy for diabetic dyslipidemia; however, for severely hypertriglyceridemic patients, fibric acid derivatives should be used. Nicotinic acid worsens hyperglycemia and, therefore, should be avoided. The value of estrogen replacement therapy in postmenopausal women with diabetes has not been established.

Diabetes Mellitus, Type 1↗

Understanding Interphase Boundary Dynamics by In Situ High-Resolution and Energy-Filtering Transmission Electron Microscopy and Real-Time Image Simulation.

: This study discusses the use of in situ high-resolution transmission electron microscropy (HRTEM) techniques to determine the structure, composition, and interphase boundary dynamics during phase transformations at the atomic level. Three main in situ HRTEM techniques are described: (1) in situ HRTEM dynamic studies that are performed on the same precipitate plates from different viewing directions to determine the three-dimensional structure of the interfaces; (2) in situ compositional mapping of precipitate interfaces obtained by energy-filtering TEM experiments at temperature in a HRTEM, and (3) real-time HRTEM image simulations that are being created for comparison with and interpretation of experimental in situ HRTEM dynamic observations. The results from these studies demonstrate that it is possible to understand the mechanisms and kinetics of interphase boundary motion at the atomic level.

Journal Article↗

Localization of the gene for familial partial lipodystrophy (Dunnigan variety) to chromosome 1q21-22.

Obesity is strongly implicated in the pathophysiology of insulin resistance, diabetes mellitus and dyslipidemia. The mechanisms, however, by which obesity causes these complications are not known. The study of single-gene disorders affecting adipose tissue may elucidate some of the mechanisms involved in these processes. Familial partial lipodystrophy, Dunnigan variety, (FPLD, OMIM 308980) is an autosomal-dominant condition characterized by marked loss of subcutaneous adipose tissue affecting the trunk and extremities but with excess fat deposition in the head and neck areas. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus, dyslipidemia and acanthosis nigricans. The genetic basis of FPLD is unknown. We carried out a genome-wide scan with a set of highly polymorphic short tandem-repeats (STR) in individuals from five well-characterized pedigrees and mapped the FPLD locus to chromosome 1q21-22. The maximum two-point lod score obtained with a highly polymorphic microsatellite at D1S2624 at theta(max)=0 was 5.84. Multipoint-linkage analysis yielded a peak lod score of 8.25 between D1S305 and D1S1600. There was no evidence for genetic heterogeneity (alpha=1) in the pedigrees.

Chromosomes, Human, Pair 1↗

High-monounsaturated-fat diets for patients with diabetes mellitus: a meta-analysis.

The most recent position statement on nutrition from the American Diabetes Association recommends an individualized approach to nutrition that is based on the nutritional assessment and desired outcomes of each patient and that takes into consideration patient preferences and control of hyperglycemia and dyslipidemia. To achieve these nutritional goals, either low-saturated-fat, high-carbohydrate diets or high-monounsaturated-fat diets can be advised. A meta-analysis of various studies comparing these two approaches to diet therapy in patients with type 2 diabetes revealed that high-monounsaturated-fat diets improve lipoprotein profiles as well as glycemic control. High-monounsaturated-fat diets reduce fasting plasma triacylglycerol and VLDL-cholesterol concentrations by 19% and 22%, respectively, and cause a modest increase in HDL-cholesterol concentrations without adversely affecting LDL-cholesterol concentrations. Furthermore, there is no evidence that high-monounsaturated-fat diets induce weight gain in patients with diabetes mellitus provided that energy intake is controlled. Therefore, a diet rich in cis-monounsaturated fat can be advantageous for both patients with type 1 or type 2 diabetes who are trying to maintain or lose weight.

Blood Glucose↗