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Data voluntarily supplied by industry were examined to evaluate the success of commercial weight loss programs and products. Information about the safe loss of weight, the maintenance of this lowered weight, and resultant health benefits were reviewed. Information was received from companies that produce over-the-counter preparations designed for persons with a small weight loss goal and from physician-supervised programs for morbidity obese persons placed on very-low-calorie diets. Regardless of the products used, successful weight loss and control was limited and required individualized programs consisting of restricted caloric intake, behavior modification, and exercise. Although some manufacturers of physician-supervised weight loss products for obese persons hav defined the effectiveness of their programs with controlled clinical studies, other industry programs have only begun to accurately assess their effectiveness or safety. Given the importance to public health of reducing obesity, rigorous studies on current weight control practices should be pursued aggressively. [ABSTRACT FROM AUTHOR]

The use of high fructose corn syrup (HFCS) has increased over the past several decades in the United States while overweight and obesity rates have risen dramatically. Some scientists hypothesize that HFCS consumption has uniquely contributed to the increasing mean body mass index (BMI) of the U.S. population. The Center for Food, Nutrition, and Agriculture Policy convened an expert panel to discuss the published scientific literature examining the relationship between consumption of HFCS or "soft drinks" (proxy for HFCS) and weight gain. The authors conducted original analysis to address certain gaps in the literature. Evidence from ecological studies linking HFCS consumption with rising BMI rates is unreliable. Evidence from epidemiologic studies and randomized controlled trials is inconclusive. Studies analyzing the differences between HFCS and sucrose consumption and their contributions to weight gain do not exist. HFCS and sucrose have similar monosaccharide compositions and sweetness values. The fructose:glucose (F:G) ratio in the U.S. food supply has not appreciably changed since the introduction of HFCS in the 1960s. It is unclear why HFCS would affect satiety or absorption and metabolism of fructose any differently than would sucrose. Based on the currently available evidence, the expert panel concluded that HFCS does not appear to contribute to overweight and obesity any differently than do other energy sources. Research recommendations were made to improve our understanding of the association of HFCS and weight gain.

With the approval for use in foods in Japan and the United States, the use of diacylglycerol (DAG) oil in fat-based products may become extensive due to equivalent physicochemical properties to conventional triacylglycerol (TAG) oil. The objective of the present study was to compare the effects of high-dose consumption of DAG oil in humans with that of TAG oil. In a double-blind controlled parallel trial, moderately lean men (n=42) and women (n=39) consumed either DAG or TAG at a dose of approximately 0.5 g/kg body weight/day as part of their diet for 12 weeks. All subjects completing the study tolerated the test oils well and showed no overt effects. Total caloric and fat intake remained constant and showed no significant differences between the groups. There was no significant difference in the occurrence of clinical signs and physical complaints related to test oil consumption. Although some statistically significant effects were reported in hematological and serum chemistry parameters in both DAG and TAG groups, none of these reported changes were considered biologically significant. Overall, this 12-week clinical study revealed no significant or treatment-related adverse effects of DAG oil consumed at a dose of 0.5 g/kg of body weight/day as part of the diet.

The science and policy underlying food labeling and food fortification have evolved over the past 30 years to a point where dietary guidance and nutrition labeling now provide consumers with highly sophisticated, very specific information about links between diet and health. The focus was once on prevention of nutrient deficiency diseases, but today it is on reducing the risk of chronic diseases and health-related conditions. The Nutrition Labeling and Education Act of 1990, with its provisions for authorization of health claims on food labels, has provided a gateway through which a broader realm of nutrition and health information can be made available to consumers. However, the interpretation and implementation of the health claim provisions must evolve, based on a strong foundation of supporting science, so that industry may more readily make health information available to consumers in a form that is easily understood and effectively used in making their dietary choices. We must develop a database to support claims of beneficial effects of food components. We must be assured that the beneficial effects are not outweighed by safety concerns. And we must develop an environment that is conducive to conducting the research to develop these data. This can only be accomplished through the collaborative efforts of industry, academia, consumers and public health agencies.

Fat substitutes, in theory, may provide special health benefits to certain population segments. The most probable benefits are a reduction in total fat intake and a subsequent reduction in intake of calories from fat. Whether individuals who consume high intakes of fat substitutes that are partially or totally nondigestible also benefit from lower calorie intake on a long-term basis is unknown. It is likely that many individuals will compensate by increasing total food intake to maintain calorie intake. Consumption of fat substitutes presents nutrition problems. Those fat substitutes that are partially or totally nondigested may reduce the bioavailability of other nutrients. Similarly, fat substitutes may have adverse effects on normal gastrointestinal tract function or intestinal tract flora. Unlike other functional food additives, fat substitutes can make up a significant portion of the total diet. For this reason, traditional safety factors cannot be applied. Consequently, more reliance on data from clinical studies involving human subjects and requirements for postmarket surveillance will be necessary as part of the approval process.

Introduction: Nowadays, fructose uses dramatically increased in form of High-Fructose Corn Syrup (HFCS) found in juices and packed food. Sustained fructose utilization is detrimental to long-term human health. Objectives: To assess the additive effects of HFCS during 7,12-Dimethylbenz(a)Anthracene (DMBA)-induced Hamster Buccal Pouch Carcinogenesis (HBPCs) model. Materials and Methods: The animals were separated into eight groups: Group I; vehicle control; Group II (0.5% DMBA); Group III and IV (HFCS 8% and 25%); Group V (Sucrose 10%); Group VI and VII (0.5% DMBA+HFCS 8 and 25%) and VIII group (0.5% DMBA+Sucrose 10%) respectively for 14 weeks. After the 14th week of treatment; the tumor morphology, buccal histopathology, and biochemical markers were measured and compared with carcinogenic control as well as vehicle control. Observations and Results: The buccal pouch of golden Syrian hamsters developed well-differentiated squamous cell carcinoma after getting topical applications of 0.5% DMBA in liquid paraffin three times a week for 14 weeks. Although DMBA treatment alone caused 100% tumor development in hamsters, drinking water administration of HFCS at a concentration of 25%/kg body weight (b.w.) to DMBA-treated hamster greatly accelerated the development of oral tumors. Additionally, during DMBA-induced oral carcinogenesis, HFCS moderatingly increased the lipid peroxidation by-products, decreased the status of enzymatic and non-enzymatic antioxidants, modulated the levels of phase I and phase II detoxification agents, and favored the excretion of carcinogenic metabolite. Conclusion: The present study concludes that the additive effect of HFCS relies on its altered peroxidative and antioxidant function as well as effects on phase I and II detoxification enzymes during DMBA-induced hamster buccal pouch carcinogenesis. Taken together the current study described that HFCS induced oral tumour development. From this study we suggested HFCS usage to be curtailed. [ABSTRACT FROM AUTHOR]

Heart failure (HF) can be caused by a variety of causes characterized by abnormal myocardial systole and diastole. Ca 2+ current through the L-type calcium channel (LTCC) on the membrane is the initial trigger signal for a cardiac cycle. Declined systole and diastole in HF are associated with dysfunction of myocardial Ca 2+ function. This disorder can be correlated with unbalanced levels of phosphorylation / dephosphorylation of LTCC, endoplasmic reticulum (ER), and myofilament. Kinase and phosphatase activity changes along with HF progress, resulting in phased changes in the degree of phosphorylation / dephosphorylation. It is important to realize the phosphorylation / dephosphorylation differences between a normal and a failing heart. This review focuses on phosphorylation / dephosphorylation changes in the progression of HF and summarizes the effects of phosphorylation / dephosphorylation of LTCC, ER function, and myofilament function in normal conditions and HF based on previous experiments and clinical research. Also, we summarize current therapeutic methods based on abnormal phosphorylation / dephosphorylation and clarify potential therapeutic directions., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The decrease in insulin sensitivity during the transition of preruminant calves into ruminant animals is the common denominator. Meanwhile, this adaptation predisposes dairy calves towards various health issues and metabolic disorders that occur in later life. Chromium (Cr) has been shown to potentiate insulin functioning and is thereby helpful in reducing the risk of these metabolic disorders. The aim of this study was to assess the effect of Cr supplementation on the insulin sensitivity and health status in Hariana calves during their transition period. A total of 24 preruminant Hariana calves were randomly allocated into four groups (6 calves per group) for a period of 90 days. Calves either received a basal diet devoid of supplemental Cr (control; Cr0.0 group) or were supplemented with 0.05 mg (Cr0.05 group), 0.10 mg (Cr0.10 group), and 0.15 mg (Cr0.15 group) of Cr per kg BW0.75 as Cr-picolinate (Cr-Pic). To determine the effect of Cr supplementation on the insulin response, glucose-insulin-non-esterified fatty acids (NEFAs) kinetics was studied during the intravenous glucose tolerance test (IVGTT) and oral glucose tolerance test (OGTT). A rapid glucose disappearance (p < 0.05) with unaltered insulin kinetics during IVGTT and OLTT indicates greater insulin sensitivity in calves supplemented with 0.10 and 0.15 mg of Cr per kg BW0.75. Improved insulin sensitivity in the Cr0.10 and Cr0.15 groups was further confirmed by higher (p < 0.05) values of the insulin sensitivity check index (QUICKI), revised quantitative insulin sensitivity check index (RQUICKI), and lower (p < 0.05) values of the homeostasis model assessment-insulin resistance (HOMA-IR) during IVGTT. Mean serum non-esterified fatty acids (NEFAm), and insulin receptor substrate-1 (IRS-1) levels were the highest (p < 0.05) and cortisol concentrations were the lowest (p < 0.05) in the Cr0.15 groups. Unlike IVGTT, there was no effect of treatment, period, and treatment × period interaction on mean serum glucose and insulin levels during OGTT. However, Cr-supplemented calves had a higher (p < 0.05) glucose clearance rate (gCR). Serum IRS-1 concentrations during OGTT were also higher (p < 0.05) in the Cr0.10 and Cr0.15 groups than in the other groups. Serum Cr levels increased dose dependently and were the highest (p < 0.05) in calves fed a diet supplemented with 0.15 mg Cr per kg BW0.75. There was no effect of treatment on average daily gain (ADG) and body condition score (BCS) while frequency and duration of diarrhea were lower and fecal score was better in Cr-supplemented calves. The current findings show that Cr supplementation improved glucose utilization and health status in calves during their transition period by improving insulin sensitivity. [ABSTRACT FROM AUTHOR]

Glycogen metabolism was studied in the isolated perfused liver of the monkey conceptus at 90% of gestation using an in situ recirculating perfusion system. Net uptake of glucose and galactose and the activities of the enzymes, glycogen synthetase and phosphorylase, were studied in response to varied perfusate composition. Synthetase activity was expressed as %I. the percentage of total synthetase activity in the active form. Perfusate glucose concentrations as high as 700 mg/100 ml did not lead to net glucose uptake of to an increase in the baseline %I synthetase (4 +/- 1, mean +/- SEM). In the presence of 300 mg/100 ml glucose, insulin at 10(-7) M in creased %I to 8 +/- 2, and galactose greater than 75 mg/100 ml increased %I to 8 +/- 1. The combination of galactose, glucose, and insulin increased %I to 40 +/- 5. With this latter combination, synthetase activity was proportional to perfusate glucose concentration above 100 mg/100 ml. Phosphorylase activity was diminished by either galactose or insulin, and phosphorylase activity was lowest in the group receiving galactose, glucose, and insulin. Galactose was taken up by all livers, but net glucose uptake was not observed under any condition; net hexose uptake was observed in perfusions with galactose. Glycogen levels did not vary significantly with varied perfusate composition during the 30-min perfusion periods.

With heat treatment (20 degrees C for 30 min), the glucocorticoid-receptor complex becomes 'activated' and undergoes an increase in affinity for DNA. A two-stage procedure was used to separate sequentially the rat liver glucocorticoid-receptor complex from proteins with high and low affinity for DNA. DNA-cellulose column chromatography of unheated cytosol resulted in the retention of DNA-binding proteins, but not the unactivated receptor complex. Heat treatment of the column eluate resulted in increased affinity of the receptor complex to DNA, and chromatography on DNA-cellulose then yielded receptor complex free from proteins with low affinity for DNA. Removal of DNA-binding proteins during the first chromatographic step was critically dependent on ionic conditions and the ratio of cytosol chromatographed to DNA-cellulose. A purification of 11000-fold (85% yield) was achieved by this procedure. The partially purified receptor complex was taken up by rat liver nuclei.

Near term fetal monkey livers were perfused with a closed recirculating system and a defined perfusion medium. Livers from normal fetal animals were able to release glucose rapidly into the perfusate when they were exposed to glucagon, cyclic AMP, or an aglycemic perfusate, but they did not remove glucose rapidly from the perfusate, synthesize glycogen, or activate liver glycogen synthetase in response to hyperglycemia (Figs. 1,2, and 3; Table 1). Insulin decreased glucose mobilization in response to aglycemia, but did not stimulate glucose uptake during hyperglycemia; insulin activated glycogen synthetase (Table 1; Figs. 1 and 3). Livers from fetuses of streptozotocin-treated mothers and livers from 2-week-old neonates released more glucose into the perfusate in response to aglycemia then did livers from normal fetal monkeys (Fig. 4). These observations support the possibility that neonatal monkey liver is capable of rapidly mobilizing glucose during periods of hypoglycemia but is unable to take up glucose and store glycogen rapidly during periods of hyperglycemia.

Partially purified rabbit skeletal muscle phosphorylase phosphatase (EC 3.1.3.17; phosphoprotein phosphohydrolase) was inactivated when it was incubated with exogenous cyclic AMP-dependent protein kinase (EC 2.7.1.37; ATP:protein phosphotransferase), cyclic AMP, and ATP-Mg. Subsequent separation of the phosphatase by acrylamide gel electrophoresis or sucrose density centrifugation resulted in reactivation of the enzyme. The phosphatase decreased in molecular weight from approximately 70,000 to 52,000, and a phosphorylated inhibitor with molecular weight of 26,000 was found. Reactivation of phosphatase also occurred when it was incubated with MnCl2 or trypsin. The inhibitor was effective at less than 10(-8) M and was relatively heat stable. Its activity was destroyed by tryptic digestion and by dephosphorylation by a Mn-stimulated phosphatase. These observations support the possibility that phosphorylase phosphatase activity is controlled by cyclic AMP-dependent protein kinase and a Mn-stimulated phosphatase by a reaction involving phosphorylation and dephosphorylation of a protein phosphatase inhibitor.

Daily urinary chromium (Cr) excretion of 15 healthy free-living female subjects was 0.20 +/- 0.03 microgram (mean +/- SEM) and nearly identical for 27 male subjects, 0.17 +/- 0.02 microgram. Minimum Cr absorption calculated from urinary Cr excretion was about 0.4 percent. Increasing intake fivefold by Cr supplementation led to a nearly fivefold increase in Cr excretion suggesting that the extent of absorption of supplemental inorganic chromium was similar to that from normal dietary sources. Correlations between 24-hour Cr excretion and urine volume, age, total creatinine and body weight were not found. Urinary Cr concentration of samples obtained following a morning void correlated with creatinine and Cr concentration following a glucose challenge but not with serum glucose, insulin, lipid parameters, age or body weight. Similar results were obtained for urine samples obtained from subjects during Cr supplementation. These results suggest that urinary Cr excretion does not appear to be a meaningful indicator of Cr status but is a meaningful indicator of Cr intake and that the absorption of supplemental inorganic Cr was similar to that of Cr from normal dietary sources.

Direct regulation of rat liver glycogen metabolism by glucose and galactose was studied using an isolated liver perfusion system. Activation of glycogen synthase and net glycogen synthesis increased linearly when perfusate glucose concentration was increased from 125 to 500 mg/100 ml. Galactose, rapidly taken up by isolated rat liver regardless of circulating glucose concentration, increased these responses to glucose. In the presence of galactose (greater than or equal to 5 mg/100 ml), activation of synthase and glycogen synthesis were 1.5-fold higher at any given glucose concentration. The addition of insulin did not appreciably after synthase activation by glucose and galactose. Phosphorylase activity, low at circulating glucose levels above 125 mg/100 ml, was further decreased as glucose was increased or when galactose was added to the perfusate. Release of glucose into the perfusate in response to aglycemia was increased in the presence of galactose.

A critical review composed of two parts: estimates of present levels of sugars intake and of recent trends in nutritive carbohydrate sweetener content of the food supply and a review of recent scientific literature addressing potentially adverse health effects associated with sugars consumption. The review contains an executive summary, an appendix with 75 tables summarizing the estimation of sugars intake of U.S. population groups, and over one thousand citations.

Blood galactose concentrations were measured in 55 neonates consuming at least 80 ml/kg/day of lactose-containing formula. The range of galactose concentration immediately after feeding was 0.8 to 4.2 mg/dl, with a mean of 1.5 +/- 0.2 mg/dl. Galactose concentration fell rapidly after feeding, and normal values for the population fell with a half-life of 45 minutes. Considering galactose as a potential intravenous nutrient, six glucose-intolerant premature infants were given galactose-containing solutions intravenously using a double-blind randomized crossover protocol. Infants were chosen who had sustained hyperglycemia (150 mg/dl) and glucosuria (2+ Clinitest) requiring glucose infusion at a rate below 7 mg/kg/minute for more than 24 hours. Compared to the control glucose period, intravenous alimentation with a solution containing carbohydrate as 50% glucose and 50% galactose resulted in a 65% increase in total carbohydrate infusion rate, normalization of the blood glucose concentration, and decreased glucosuria. Blood galactose concentration averaged 15 mg/dl, and no clinical or biochemical evidence of galactose toxicity was noted.

In fetal rat liver in utero, an increase in glycogen and the glycogen synthetic enzyme glycogen synthetase (EC 2.4.1.11) occurs between gestational days 17 and 19. We used an organ culture system for finding the stimulus for increased enzyme activity and defining the relationship of this increase to glycogen synthesis. In fetal-liver explants from an earlier period (gestational day 16), hydrocortisone causes an elevation in total glycogen synthetase activity. This effect, which can be blocked by actinomycin D, is strikingly similar in time course and magnitude to the normal increase in utero. However, in order for glycogen synthesis to proceed after hydrocortisone increases glycogen synthetase levels, insulin is required. Unlike hydrocortisone, insulin does not increase total glycogen synthetase; it appears to act by converting the b or phospho form of synthetase to the a or dephospho form. Insulin alone does not stimulate glycogen synthesis in explants from 16-day fetal liver, although no defect in insulin binding was demonstrable. These findings support the hypothesis that the increase in liver-glycogen synthesis during the last trimester requires glucocorticoids for the developmental induction of glycogen synthetase and insulin for activation of the enzyme.

It is generally accepted that human T-cell lymphotropic virus type III (HTL VIII) is the causative agent of acquired immunodeficiency syndrome (AIDS), but, asyet, there are no clear reasons for the different clinical manifestations of AIDS among individuals. In this article Douglas Archer and Walter Glinsmann discuss the history of AIDS and propose a link between HTLV-III infection and gastrointestinal disease processes with attendant malabsorption. They further propose that maximizing the nutritional status and minimizing the incidence of gastrointestinal infection of individuals infected with HTLV-III may prevent development of the full-blown AIDS., (Copyright © 1985. Published by Elsevier B.V.)

Administration of adrenaline to an isolated rat hindlimb preparation rapidly decreased muscle phosphorylase phosphatase (EC 3.1.3.17) activity and increased heat-stable and trypsin-labile phosphatase inhibitor activity. This was associated with increased tissue cyclic AMP concentrations, phosphorylase (EC 2.4.1.1) activation and glycogen synthase (EC 2.4.1.11) inactivation.

Two heat-stable and trypsin-labile inhibitors of phosphorylase phosphatase, designated inhibitor-1 and inhibitor-2, were partially purified from extracts of rabbit skeletal muscle by heating and coloumn chromatography using DEAE-dellulose and Bio-gel P-60. Inhibitor-1 exists in an active phosphorylated form and an inactive dephosphorylated form. The interconversion of phosphorylated inhibitor-1 and dephosphorylated inhibitor-1 is mediated by protein kinase dependent on adenosine 3':5'-monophosphate (cyclic AMP) and a Mn2+-stimulated phosphoprotein phosphatase. Inhibitory activity of inhibitor-2 is not influenced by treatment with either the kinase or the Mn2+-stimulated phosphatase. The molecular weights of inhibitor-1 and inhibitor-2 estimated by sodium dodecylsulfate-polyacrylamide gel electrophoresis are 26000 and 33000 respectively. Both inhibitor-1 and inhibitor-2 inhibit phosphorylase phosphatase by a mechanism which appears to be non-competitive with respect to the substrate phosphorylase a. Inhibitor fractions at early stages of purification also inhibit cyclic-AMP-dependent histone phosphorylation, but this kinase inhibitory activity resides with a protein moiety which is separable from inhibitor-1 and inhibitor-2.

Sharp increases in the concentration of chromium in plasma were found in five subjects with normal glucose utilization after administration of glucose by mouth. This rise was not observed in two diabetics when glucose tolerance was impaired; however, it appeared when glucose tolerance was improved and when trace amounts of trivalent chromium were given as a dietary supple-ment. The source of chromium which became elevated was most likely an internal pool. Possibly there is a relation between chromium and insulin function.

The supply of food for the world population that is increasing is one of the concerns of governments. The Food and Agriculture Organization of the United Nations assessment shows that the aquaculture industry could help meet food needs for human communities. The aquaculture industry also relies on providing a feed of high quality. Minerals are one essential component of an aquatic diet. Chromium (Cr) is a trace element that finds the form of Cr+3 (trivalent) and Cr+6 (hexavalent) in nature and food items. Studies show that exposure to Cr waterborne have toxicity effects on fish. However, oral exposure to Cr has a different impact on fish. Cr is usually involved in the metabolism of fats, carbohydrates, proteins, growth function, enzyme functions, etc. This element could play a significant role in fish nutrition and physiology. Cr as a dietary supplement can improve growth performance and adjust the metabolism of carbohydrates and lipids. However, high concentrations of Cr can be toxic to fish. Although the physiological effects of Cr on aquatic organisms are well known, there are still ambiguities in determining the appropriate concentration in the diet of some species. Maybe, the physiological response of fish depends on the concentration, origin, and chemical composition of Cr, as well as the biological and individual characteristics of the fish. Therefore, it is necessary to estimate the appropriate concentration of Cr in fish diets. This article aims to summarize the available information about the effect of Cr on various physiological indicators and fish growth. Therefore, this information may help to find the appropriate concentration of Cr in the diet. [ABSTRACT FROM AUTHOR]

Rapidly proliferating cancer cells exhibit a high energy demand. However, their utilization of the glycolytic pathway is inefficient, leading to a compensatory effect wherein cancer cells consume ten to twenty times more glucose than normal cells. In cases where glucose availability is limited due to a poorly perfused hypoxic microenvironment, cancer cells resort to alternative energy sources, including fructose. Certain tumors have been found to rely heavily on fructose, and fructose utilization contributes to pro-tumoral signaling and increased cancer risk. Over the past 70 years, dietary fructose intake has steadily increased, resulting in a rise in obesity and metabolic syndrome, both of which elevate cancer risk. In this paper, we present compelling evidence that highlights the role of fructose and the glucose transporter GLUT5 in promoting specific types of tumors. We summarize the existing evidence and pathways through which fructose contributes to cancer metabolism, particularly in cases where glucose availability is restricted. Furthermore, we propose a hypothesis that elucidates the regulation of the lipogenic phenotype by dietary fructose intake and cellular energy status. It is important to note that the effects of fructose are contextdependent, with its tumor-promoting effects varying based on the energy status of the cell. We comprehensively analyze why targeting fructose uptake and fructolysis should be important for the management of some tumors and cancer prevention. [ABSTRACT FROM AUTHOR]

Chromium(III) is extensively used as a supplement for muscle development and the treatment of diabetes mellitus. However, its mode of action, essentiality, and physiological/pharmacological effects have been a subject of scientific debate for over half a century owing to the failure in identifying the molecular targets of Cr(III). Herein, by integrating fluorescence imaging with a proteomic approach, we visualized the Cr(III) proteome being mainly localized in the mitochondria, and subsequently identified and validated eight Cr(III)-binding proteins, which are predominately associated with ATP synthesis. We show that Cr(III) binds to ATP synthase at its beta subunit via the catalytic residues of Thr213/Glu242 and the nucleotide in the active site. Such a binding suppresses ATP synthase activity, leading to the activation of AMPK, improving glucose metabolism, and rescuing mitochondria from hyperglycaemia-induced fragmentation. The mode of action of Cr(III) in cells also holds true in type II diabetic male mice. Through this study, we resolve the long-standing question of how Cr(III) ameliorates hyperglycaemia stress at the molecular level, opening a new horizon for further exploration of the pharmacological effects of Cr(III). Despite common use as a diabetes mellitus supplement, chromium(III)'s pharmacological effects remain unknown. We identified the Cr(III)-proteome in cells with a metalloproteomic approach and uncovered ATP synthase as a vital target to relieve hyperglycaemia stress. [ABSTRACT FROM AUTHOR]